Sukolrat Boonyayatra
DVM, MS
Clinic for Ruminants
Inflammation of one or more quarters of the udder
Mammae = breast
-itis = Latin suffix for inflammation
Normal
Inflamed
Swelling pain warm redness
Intramammary Infection (IMI):
Bacterial infection
Mycoplasmal infection
Mycotic (fungal) infection
Algal infection
Mechanical trauma
Thermal trauma
Predisposes the gland to IMI
Chemical insult
Mastitis accounted for 26% of the total cost of all dairy cattle diseases.
Losses from mastitis were twice as high as losses from infertility and reproductive diseases.
Sources of loss
Reduced milk production
Discarded milk
Early cow replacement costs
Reduced cow sale value
Drugs
Veterinary services labor
Active involution
High Pressure in the gland
Bacteria inside the gland
Teat dipping ceases.
Phagocytic efficiency
Increasing of immunoglobulins and lactoferrin cannot override the problems noted above.
Dry cow treatment can not reduce coliform IMI during active involution.
Reducing the period of active involution by infusing colchicine (disrupts milk secretion mechanisms) decreases
IMI during the active involution phase.
Peripartum period
Fluid volume in the gland increases
Citrate concentration rises and lactoferrin is low
Phagocytic cells efficiency
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
Teat dipping
Early lactation
Metabolically stressed
Mastitis is sometimes associated with high concentrate feeding which accompanies early lactation.
Micronutrient Observation
Se Decreased efficiency in neutrophil funtion
Improved bactericidal capabilities of neutrophils
Decreased severity and duration of mastitis
Vit E
Vit A
β -carotene
Cu
Zn
Increased neutrophil bactericidal activity
Decreased incidence of clinical mastitis
In combination with Se, decreased prevalence of IMI at calving
Decreased SCC
Moderated glucocorticoid levels
Increased bactericidal function of phagocytes
Increased mitogen-induced proliferation of lymphocytes
Deficiency decreased neutrophil killing capability
Deficiency increased susceptibility to bactericidal infection
Deficiency decreased leukocyte function
Deficiency increased susceptibility to bacterial infection
1. Multiplication of bacteria in mammary gland
2. Vasodilation
3. Increased vascular permeability
4. Swelling
5. Diapedesis
6. Phagocytosis and destruction of bacteria
7. Tissue repair
Development of mastitis and the cow
’s defense against the infection
The major routes of bacterial transmission
Categorized based on Severity of Immune
Response
Peracute Mastitis: sudden onset, severe inflammation of the udder, and serous milk-Systemic illness often precedes the symptoms manifested in the milk and mammary gland.
Acute Mastitis: sudden onset, moderate to severe inflammation of the udder, decreased production, and occurrence of serous milk/fibrin clots, Systemic signs are similar but less severe than for the peracute form.
Subacute Mastitis: mild inflammation, no visible changes in udder, but there generally are small flakes or clots in the milk, and the milk may have an off-color. There are no systemic signs of illness.
Chronic Mastitis: Chronic mastitis may persist in a subclinical form for months or years with occasional clinical flare-ups. Treatment usually involves treating the clinical flare-ups, or culling the cow from the herd.
Subclinical Mastitis: the most common form of mastitis, 15x40 X more common than clinical mastitis, no gross inflammation of the udder and no gross changes in the milk, decreased production and decreased milk quality
Elevated Somatic Cell Count
Abnormal Milk
Abnormal Udder
~98-99% White Blood Cell + 1-2% Epithelial cells from milk-secreting tissue
Cow’s natural defense mechanism
Normal or uninfected cow: 50,000-200,000 cells/ml
>200,000 cells/ml: the likelihood of infection increase
Prevalence of subclinical mastitis in Chiang Mai may be exceed 80%.
1 clinical mastitis : 15-40 subclinical mastitis
Subclinical mastitis results in INCREASES in undesirable milk components and
DECREASES in the desirable components.
Pasteurized milk that is processed from raw milk with a somatic cell count below 250,000 has a significantly longer shelf-life than products made from milk with a somatic cell count above 500,000.
Lactose (good)
Total proteins (good)
Casein (good)
Immunoglobulins (bad)
Solids not fat (good)
Total solids (good)
Fat (good)
Lipase (bad)
Sodium (bad)
Chloride (bad)
Calcium (good)
Phosphorus (good)
Potassium (good)
Trace minerals (bad)
Cheese (good)
Heat stability (good)
Decreased 5 to 20%
Decreased slightly
Decreased 6-18%
Increased
Decreased up to 8%
Decreased 3 t0 12%
Decreased 5 to 12%
Increased rancidity
Increased
Increased
Decreased
Decreased
Decreased
Slight increase
Decreased curd strength, fat and yield
Reduced
Animal health
Loss of functional quarter
Lowered milk production
Death of cow
Human health
Poor quality milk
antibiotic residues in milk
~ 90 -95% of all mastitis cases
Udder appears normal
Milk appears normal
Elevated SCC (score 3-
5)
Lowered milk output
(~ 10%)
Longer duration
Clinical Mastitis
~ 5 - 10% of all mastitis cases
Inflamed udder
Clumps and clots in milk
Acute type major type of clinical mastitis bad milk loss of appetite depression prompt attention needed
Chronic type bad milk cow appears healthy
Bacteria ( ~ 70%)
Yeasts and molds ( ~ 2%)
Unknown ( ~ 28%)
physical trauma
weather extremes
Infected udder
Environment
bedding
soil
water
manure
Replacement animals
Cow
Predisposing conditions
Existing trauma (milking machine, heat or cold, injury)
Teat end injury
Lowered immunity (following calving, surgery)
Nutrition
Organisms
Environment
Organisms invade the udder through teat canal
Migrate up the teat canal and colonize the secretory cells
Colonized organisms produce toxic substances harmful to the milk producing cells
The cow’s immune system send white blood cells (Somatic cells) to fight the organisms recovery clinical subclinical
Contagious microorganisms
Staphylococcus aureus
Streptococcus agalactiae
Mycoplasma bovis
Corynebacterium bovis
Environmental microorganisms
Environmental streptococci
Coliform
Opportunistic microorganisms
Staphylococcus spp.
(CNS)
Others
Pseudomonas aeruginosa
Actinomyces pyogenes
Nocardia Species
Environmental
S. uberis
S. dysgalactiae
S. equinus
More subclinical mastitis
Environment
Predominant early and late lactation
Contagious
S. agalactiae
Clinical mastitis
Resides in the milk and on the surface of the milk channel
Cannot invade the tissue
Accumulate Neutrophils
Ducts and acinar epithelium damage
Inter-alveolar tissue fibrosis
loss of secretory function
Treated easily with penicillin
Staph aureus
Gangrenous mastitis: alpha toxin
Spread by milking equipment and milker’s hands
Fibrous tissue replacement low production
Poor response to ABO
Dry cow therapy
Persistent, difficult to eliminate
Other staph
Found normally on skin
Lowers milk yield
Elevated SCC
Easily responds to antibiotics
Relapse frequently seen
Fig. 1. Mammary parenchyma from which coagulase-negative
Staphylococcus was isolated, showing the presence of mononuclear cells. HE. 660
Fig. 2. Mammary parenchyma from which coagulase-negative
Staphylococcus was isolated, showing the presence of neutrophils within the alveolar lumen. HE. 660 .
Fig. 3. Mammary parenchyma from which Prototheca sp. was isolated, showing the micro-organisms within the alveolar lumen. HE. 660 .
The cocci in the lesions of the mammary glands show a positive reaction to antibody against
Staph.aureus
(ABC X 200)
a.
The bacteria were round or oval in shape, showing a thick cell wall, characteristic of gram-positive bacteria
(TEM. X 40,000) b. Fibrous material (arrows) stained by ruthenium-red, around the bacterial cell wall, which forms a capsule
(TEM.X 250,000)
Severe necrosis of interlobular and intralobular ducts
The lesions affected the intralobular duct, intralobular duts and alveoli
(Azan x 30).
Bacterial clumps(arrows) surrounded by alveolar epithelial cells undergoing necrosis
Thrombus(*)is seen in the blood vessel(He x 100).
Groups of organisms
E. coli, Klebsiella, Enterobacter
Environmental source (manure, bedding, barns, floors and cows)
Coliforms cause acute clinical mastitis
Multiply rapidly with low SCC
Endotoxin releasing
High temp, and inflamed quarter
Watery milk with clots and pus
Toxemia
The udder can be gradually return to normal without fibrosis
Pseudomonas aeruginosa
Out breaks of clinical mastitis or subclinical mastitis
Similar pathogenesis to coliform mastitis
Severe endotoxaemia can occur.
Serratia
Out breaks of clinical mastitis
Summer mastitis
Most common in Europe
Actinomyces pyogenes + Peptostreptococcus indolicus
Non-lactating heifers and cows at pasture in the summer months and more common during wet weather
Fly borne ??
Severe systemic reaction and Loss function
Abcess develop
Mycoplasma mastitis
Clinically severe mastitis
Rarely systemic involvement
All ages & all stages of lactation
Post calved cows show more severe signs.
Long-term persistence in udder (up to 13 mths)
Some cows can shed the organism without clinical signs.
Normal secretion in the early stage of infection
Flaky material settles out leaving a turbid
Whey-like supernatant fluid
Very high SCC
Physical examination
Signs of inflammation
Empty udder
Differences in firmness
Unbalanced quarters
Cowside tests
California Mastitis test
Cultured Analysis
The most reliable and accurate method
Clinical mastitis
Strip quarter every 2 hours
Oxytocin valuable
high temp, give NSAIDs
Seek veterinary assistance
Treatment with penicillins
Subclinical mastitis
Questionable
Stanchion/ Tie stall
Ware gloves
Wipe off excess dry manure, straw and bedding
Strip each teat into a stripcup
Dip teats with an approved pre-dip
Allow the pre-dip to react for at least 30 sec.
Parlor
Wear Gloves
Wipe off excess dry manure, straw and bedding
Strip each teat into a stripcup
Dip teats with an approved pre-dip Dip 3-4 cows
Allow the pre-dip to react for at least 30 sec.
Stanchion/ Tiestall
Parlor
Clean teat and teat ends using single paper towel or individual towel cloth
The teats must be dried for at least
clean teat and teat ends
The teats must be dried for at least 15 sec
Attach milking machines immediately after teats are dried
Dip teats with post-dip immediately after milking
Visualization and palpation of the udder
Detection of Somatic Cells
California Mastitis Test
N-acetylß-D-glucosaminidase (NAGase)
- a lysosomal enzyme which increases in milk when mastitis is present
Electrical conductivity: Sodium and Chloride ions
A radial immunodiffusion test : Serum albumin concentration increases if epithelium damage is present.
An anti-trypsin test: Anti-trypsin activity tends to naturally high at the beginning of a lactation the values are high only if serum anti-trypsin has leaked through damaged mammary epithelium.
The CMT reagent reacts with genetic material of somatic cells present in milk to form a gel.
A plastic paddle having four shallow cups marked A, B,
C and D for easy identification of the individual quarter.
Approximately 1/2 teaspoon (2 cc) of milk is. An equal amount of the CMT reagent is added to the milk.
A circular rotating to thoroughly mix the contents. Score in approximately ten seconds while still rotating.
Read the test quickly as the reaction tends to disintegrate after about 20 seconds.
Rinse the paddle thoroughly with water and it is ready for the next test.
Fairly accurate in measuring SCC in milk
Primarily developed for sampling quarters, it can also be used on "bucket" and "bulk tank" milk samples.
Foreign material does not interfere with the test.
It is inexpensive, simple, and little equipment is needed.
Easy clean-up after each test--simply rinse with water.
Environmental temperature changes have little effect on the CMT as long as the milk has been refrigerated and is not over two days old.
Herd mastitis levels can be estimated from tank CMTs. A
CMT of 2 or 3 on tank milk indicates a probable high percent of infected cows.
Scoring the test may vary between individual testers. It is necessary to be as consistent as possible to insure uniform results.
Scores represent a range of leucocyte content rather than an exact count.
False positive reactions occur frequently on cows that have been fresh less than ten days, or on cows that are nearly dry. These animals should be tested closer to the middle of the lactation.
Occasionally, acute clinical mastitis milk will not score positive due to the destruction of leucocytes by toxins
(poisons) from the infecting organism.
2
3
1
T
0
CMT score
Interpretation Visible reaction Total cell count
(/ml)
Negative Milk fluid and normal 0-200,000
0-25% neutrophils
Trace Slight precipitation 150,000-500,000
30-40% neutrophils
Weak positive
Distinct positive
Distinct precipitation but no gel formation
Mixture thickens with a gel formation
400,000-1,500,000
40-60% neutrophils
800,000-5,000,000
60-70% neutrophils
Strong positive Viscosity greatly increased.
Strong gel that is cohesive with a convex surface.
>5,000,000
70-80% neutrophils
Step 1
Educate owners and milkers about implementing a standardized milking procedure (Benefits !!!!!!)
IF a dairy farm initiates and shows sustained interest
Establish ground rules
They will have to be proactive and adopt changes
TEAM EFFORT !!!
STEP TWO
Establish a team ( owner, milkers, veterinarian, facilitator)
Mission statement
Goals and timeline
Written Procedures
Protocols
Critical Limits ( SCC > 250,000)
Recording Keeping
Milking time/milking
Bulk Tank Temp; end of 1 hr of milking
Sanitation
Schedule team meetings to review the process
STEP THREE
Train milkers and owners in implementing the standardized milking procedure
STEP FOUR
Monitor the application of the standardized milking procedure
Floor tests (each step is a critical point !)
Laboratory tests (SPC or BTSCC)
Monitor records
STEP FIVE
Establish corrective actions to be implemented if milk quality critical limits have exceeded.
1. Mastitis (Udder infection)
2. Teat or udder injury
3. Number of quarters with mastitis
4. Age of cow
5. Stage of lactation
6. Season
7. Stress
8. Day to day variation
9. Technical factors
10. Management factors
1. Milk Culture and Sensitivity Testing
2. Treatment During Lactation
3. Drying Cows Off Early
4. Culling
High SCC >500,000 cells/ml
Very useful when:
High SCC two or more tests
Beginning of lactation
Strep. agalactiae infection
Very few cases of subclinical mastitis
High SCC vs culture vs sensitivity
The best method of eliminating infection
High SCC and relatively low production
There is evidence to suggest that a repeat dry treatment 3 weeks after the first therapy could increase success rate.
Teat dipping for 10 days after lasting milking and for 10 days prior to calving
Persistently high SCC from lactation to lactation
Staph. aureus or Mycoplasma spp.
Milk production
High SCC cow could be milked last or the milking machines could be sanitized after milking.
Mastitis Bulk Tank Culture Report Interpretation
Type of Bacteria Usual Infection
Cause
Strep agalactiae Infected udders of other cows in herd
Staph aureus Infected udders of other cows, contaminated bedding from milk of infected cows
Major Means of Spread
Cow-to-cow by contaminated udder wash
Cow-to-cow by contaminated udder wash rag, milker’s hands contaminated milking equipment , and improperly functioning equipment
Mastitis Control
Use separate towels to wash/dry; Teat dipping; dry cow treatment; eradicate in special cases
Use separate towels to wash/dry; Teat dipping; dry cow treatment; milk infected cow last, cull chronically infected cows
Mycoplasma Infected udders of other cows, often from infected purchased cows/heifers
Cow-to-cow by hands of milkers, equipment, and common towels. Aerosol transmission from animals with respiratory signs may also occur. Or the bacteria can move from a respiratory tract infection to the udder or joints.
Careful purchasing of replacement cattle, using bulk tank and cow culturing to monitor herd status and clinical cows. Use separate towels to wash/dry; teat dipping; dry cow treatment; milk infected cows last, cull any positive clinical case.
Mastitis Bulk Tank Culture Report Interpretation
Type of Bacteria Usual Infection
Cause
Non-ag Streps
Coliforms
Staph species
Major Means of Spread Mastitis Control
Environment of cow Environment of the cow by; wet dirty lots, contaminated bedding, milking wet cows, poor cow prep, milking machine air slips
Environment of cow Environment of the cow by; wet dirty lots, contaminated bedding, milking wet cows, poor cow prep, milking machine air slips. Hot humid weather.
Environment of cow Poor teat dip coverage, poor cow prep, old bedding.
Improve stall and lots sanitation; milk clean dry cows, avoid air leaks and liner slips, changes bedding frequently. Keep cows standing after milking.
Improve stall and lots sanitation; milk clean dry cows, avoid air leaks and liner slips, changes bedding frequently. Keep cows standing after milking.
Consistent teat dipping, adequate cow prep, and more frequent bedding change.
1. Provide Cows with a Clean, Stress-Free
Environment
2. Check Foremilk and Udder for Mastitis
3. Wash Teats and Lower Surface of the Udder with a Warm Sanitizing Solution
4. Use a Premilking Teat Dip (Optional)
5. Dry Teats Thoroughly
6. Attach Teat Cups within 1 min.
7. Adjust Milking Units as Necessary
8. Shut Off Vacuum Before Removing Teat Cups
9. Dip Teats with a Safe and Effective Teat Dip
10. Disinfect Teat Cups Between Cows (Optional)
Problem Solving Techniques
One or more specialists: vet, fieldman, extension agent or milking machine dealer
A visual inspection of the general environment
Good detectives
Specific approach
High Incidence of Clinical Mastitis and High SCC
Detection and discarding of visibly abnormal milk.
Not milking fresh cows with cows that have clinical mastitis
Collection of milk samples and culturing in a diagnostic laboratory.
Treatment of selected cows, especially those infected with
Streptococcus agalactiae .
Culling of cows with chronic infections, particularly those caused by Staphylococcus aureus , environmental streptococci, Nocardia asteriodes , and Mycoplasma species.
Drying off of selected cows and dry treating.
Correction of deficiencies in management and environment.
(Continued)
Upgrading of milking equipment
Correction of deficiencies in milking hygiene.
Improvement in the manner in which milking machines are used.
Initiation of predipping.
Strengthening of postmilking teat dip procedures.
Arranging for fresh feed to be available when cows exit the milking parlor or barn so they will be encouraged to stand for at least 1 hour after milking to provide time for the teat canal to close tightly.
Segregation of infected cows.
Initiation of backflushing, particularly if the problem is caused by contagious microorganisms such as
Staphylococcus aureus , Streptococcus agalactiae , or
Mycoplasma species.
High Bacteria Counts
>10,000 /ml, Streptococci >75% Infected Udder
Streptococci < 25% Improper Cleaning of Milking
Equipment, Poor Udder Preparation and Poor Cooling of
Milk
High Streptococci & High Staphylococci + Coliforms +
Spore Formers + Other Organisms A dual problem of infected cows and poor udder preparation.
>15,000 /ml of Staphylococci Poor cooling of milk
High coliform counts Broken teat cup liners, low water temperature, milkstone on milk-contact surfaces and failure to use correct chemicals for cleaning milking equipment
Large number of coliforms, staphylococci, and environmental streptococci Faulty cooling of the milk
1. Milk cow with clean, dry teats and teat ends.
Impact: Milk quality, environmental mastitis, liner slips, milk out and parlor throughput
2. Prevent transfer of pathogens from cow to cow during milking.
Impact: Contagious mastitis, milk quality
3. Prevent injury to the teats during milking.
Impact : Mastitis, milk out, parlor throughput
4. Provide an environment that allows the cows to remain clean between milking.
Impact: Environmental mastitis, milk quality, parlor throughput, cow comfort
5. Early detection of new infections (clinical and subclinical).
Impact : Response to treatment, chronic infections, culling
6. Proper use of medications.
Impact : Success of treatment, cost control, residues in milk and meat
7. Control duration of infections.
Impact : Decreased prevalence, decreased culling
8. Monitor mastitis status.
Impact: Prevent outbreaks, culling information
9. Raise mastitis free replacements.
Impact : Permit culling for production, reduced herd prevalence
10. Assume all purchased replacements are infected.
Impact: Control introduction of new pathogens
11. Provide adequate nutrition to preclude increased susceptibility to mastitis.
Impact: Control new infection rate
12. Fly control.
Impact : Teat end injury, new infection rate
13. Provide routine milker training
Impact: All areas of mastitis prevention and control, milk quality
14. Assigned responsibilities for all areas of mastitis prevention.
Impact : Job knowledge, shared responsibility, improved compliance