Transcript Bovine Mastitis - Chiang Mai University

Bovine Mastitis
Sukolrat Boonyayatra
DVM, MS
Clinic for Ruminants
What’s mastitis ?
Inflammation of one or more quarters of
the udder
Mammae = breast
-itis = Latin suffix for
inflammation
Normal
Inflamed
Swelling
pain
warm
redness
Causes
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Intramammary Infection (IMI):
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Bacterial infection
Mycoplasmal infection
Mycotic (fungal) infection
Algal infection
Mechanical trauma
Thermal trauma
Chemical insult
Predisposes
the gland to IMI
Economic Losses
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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
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Reduced milk production
Discarded milk
Early cow replacement costs
Reduced cow sale value
Drugs
Veterinary services
labor
Determinants of Mastitis
Timing of infection and stage of
lactation
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Active involution
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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.
Timing of infection and stage of
lactation
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Peripartum period
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Fluid volume in the gland increases
Citrate concentration rises and lactoferrin is low
Phagocytic cells efficiency
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High immunoglobulin concentrations in the gland at this
time are not effective in preventing new IMI.
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IgG1 is not normally an effective opsonin in the mammary
gland.
Antibiotic concentration
Teat dipping
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Timing of infection and stage of
lactation
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Early lactation
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Metabolically stressed
Mastitis is sometimes associated with high
concentrate feeding which accompanies early
lactation.
Nutrition and Mastitis
Micronutrient
Observation
Se
Decreased efficiency in neutrophil funtion
Improved bactericidal capabilities of neutrophils
Decreased severity and duration of mastitis
Vit E
Increased neutrophil bactericidal activity
Decreased incidence of clinical mastitis
In combination with Se, decreased prevalence of IMI at calving
Vit A
Decreased SCC
Moderated glucocorticoid levels
β-carotene
Increased bactericidal function of phagocytes
Increased mitogen-induced proliferation of lymphocytes
Cu
Deficiency decreased neutrophil killing capability
Deficiency increased susceptibility to bactericidal infection
Zn
Deficiency decreased leukocyte function
Deficiency increased susceptibility to bacterial infection
Inflammation of Mammary gland
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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
Mastitis Clinical Syndromes
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Categorized based on Severity of Immune
Response
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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.
Mastitis Clinical Syndromes
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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.
Mastitis Clinical Syndromes
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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
Somatic Cell Count
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~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
Effects on Milk Quality
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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.
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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)
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Heat stability (good)
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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
What are the health concerns of mastitis ?
Animal health
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Loss of functional quarter
Lowered milk production
Death of cow
Human health
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Poor quality milk
antibiotic residues in milk
How severe can mastitis be ?
Subclinical Mastitis
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~ 90 -95% of all mastitis
cases
Udder appears normal
Milk appears normal
Elevated SCC (score 35)
Lowered milk output
(~ 10%)
Longer duration
Clinical Mastitis
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~ 5 - 10% of all mastitis
cases
Inflamed udder
Clumps and clots in milk
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Acute type
major type of clinical
mastitis
bad milk
loss of appetite
depression
prompt attention needed
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Chronic type
bad milk
cow appears healthy
What causes mastitis ?
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Bacteria ( ~ 70%)
Yeasts and molds ( ~ 2%)
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Unknown ( ~ 28%)
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physical
trauma
weather extremes
Where do these organisms come from ?
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Infected udder
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Environment
bedding
soil
water
manure
Replacement animals
How does mastitis develop ?
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Cow
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Predisposing conditions
Existing trauma (milking machine, heat or cold, injury)
Teat end injury
Lowered immunity (following calving, surgery)
Nutrition
Organisms
Environment
Process of infection
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
Organisms
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Contagious microorganisms
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Environmental microorganisms
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Environmental streptococci
Coliform
Opportunistic microorganisms
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Staphylococcus aureus
Streptococcus agalactiae
Mycoplasma bovis
Corynebacterium bovis
Staphylococcus spp. (CNS)
Others
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Pseudomonas aeruginosa
Actinomyces pyogenes
Nocardia Species
Bacterial Infection: Streptococci
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Environmental
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S. uberis
S. dysgalactiae
S. equinus
More subclinical mastitis
Environment
Predominant early and late
lactation
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Contagious
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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
Bacterial Infection: Staphylococci
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Staph aureus
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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
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Other staph
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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).
Bacterial Infection: Coliforms
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Groups of organisms
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E. coli, Klebsiella, Enterobacter
Environmental source (manure, bedding, barns,
floors and cows)
Coliforms cause acute clinical mastitis
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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
Bacterial Infection: Other organisms
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Pseudomonas aeruginosa
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Serratia
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Out breaks of clinical mastitis or subclinical mastitis
Similar pathogenesis to coliform mastitis
Severe endotoxaemia can occur.
Out breaks of clinical mastitis
Summer mastitis
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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
Bacterial Infection: Other organisms
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Mycoplasma mastitis
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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
How is mastitis diagnosed ?
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Physical examination
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Signs of inflammation
Empty udder
Differences in firmness
Unbalanced quarters
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Cowside tests
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California Mastitis test
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Cultured Analysis
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The most reliable and
accurate method
Treatment
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Clinical mastitis
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Strip quarter every 2 hours
Oxytocin valuable
high temp, give NSAIDs
Seek veterinary assistance
Treatment with penicillins
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Subclinical mastitis
Questionable
กล้ามเนื้อหูรูด
รู หวั นม
สอดปลายเข็มยาว1/8 – 1/4 นิ้ว
ผ่านทางรู หวั นมเท่านั้น
ปล่อยยาบางส่ วนที่ตาแหน่งติดรู หวั นม
และปล่อยยาที่เหลือทั้งหมด
ที่ตาแหน่งห่างออกไป
Partial Insertion
เข็มสั้น
เข็มยาว
ห้ามสอดเข็มยาวเข้าจนสุ ดรู หวั นม
เพราะจะทาลายไขที่ปิดรู หวั นม
ทาให้เชื้อภายนอกมีโอกาสเข้าสู่เต้านม
ได้ง่ายยิง่ ขึ้น
Standardized Milking Procedures
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Stanchion/ Tie stall
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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.
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Parlor
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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.
Standardized Milking Procedures
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Stanchion/ Tiestall
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Parlor
Clean teat and teat ends using single
paper towel or individual towel clo
 Return to the first cow and
The teats must be dried for at least 15 clean
sec teat and teat ends
Attach milking machines immediately after
are dried
usingteats
a single
paper towel
Dip teats with post-dip immediately after
or milking
individual towel cloth
 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
Detection of Mastitis
Visualization
and palpation of the udder
Detection
of Somatic Cells
California Mastitis Test
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N-acetyl-ß-D-glucosaminidase (NAGase)
- a lysosomal enzyme which increases in milk
when mastitis is present
Indirect chemical tests to detect mastitis
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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.
California Mastitis Test (CMT)
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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.
Advantages of CMT
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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.
Disadvantages of CMT
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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.
Correlation between the California mastitis
test result and the somatic cell count.
CMT Interpretation
score
Visible reaction
Total cell count
(/ml)
0
Negative
Milk fluid and normal
0-200,000
0-25% neutrophils
T
Trace
Slight precipitation
150,000-500,000
30-40% neutrophils
1
Weak positive
Distinct precipitation but no
gel formation
400,000-1,500,000
40-60% neutrophils
2
Distinct
positive
Mixture thickens with a gel
formation
800,000-5,000,000
60-70% neutrophils
3
Strong positive Viscosity greatly increased. >5,000,000
Strong gel that is cohesive 70-80% neutrophils
with a convex surface.
Steps involved in employing HACCP-based
concepts for establishing proper milking
procedures
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Step 1
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Educate owners and milkers about implementing
a standardized milking procedure (Benefits !!!!!!)
IF a dairy farm initiates and shows sustained
interest
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Establish ground rules
They will have to be proactive and adopt changes
TEAM EFFORT !!!
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STEP TWO
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Establish a team ( owner, milkers, veterinarian,
facilitator)
Mission statement
Goals and timeline
Written Procedures
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Recording Keeping
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Protocols
Critical Limits ( SCC > 250,000)
Milking time/milking
Bulk Tank Temp; end of 1 hr of milking
Sanitation
Schedule team meetings to review the process
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STEP THREE
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STEP FOUR
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Train milkers and owners in implementing the
standardized milking procedure
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
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Establish corrective actions to be implemented if
milk quality critical limits have exceeded.
Factors Affecting Somatic Cell Counts
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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
Uses of SCC on Individual Cows for
Management Decisions
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1. Milk Culture and Sensitivity Testing
2. Treatment During Lactation
3. Drying Cows Off Early
4. Culling
1. Milk Culture and Sensitivity Testing
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High SCC >500,000 cells/ml
Very useful when:
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High SCC two or more tests
Beginning of lactation
2. Treatment During Lactation
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Strep. agalactiae infection
Very few cases of subclinical mastitis
High SCC vs culture vs sensitivity
3. Drying Cows Off Early
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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
4. Culling
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Persistently high SCC from lactation to
lactation
Staph. aureus or Mycoplasma spp.
Milk production
5. Milking Routine
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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
Major Means of Spread
Mastitis Control
Strep agalactiae
Infected udders of
other cows in herd
Cow-to-cow by contaminated
udder wash
Use separate towels to
wash/dry; Teat dipping; dry
cow treatment; eradicate in
special cases
Staph aureus
Infected udders of
other cows,
contaminated
bedding from milk
of infected cows
Cow-to-cow by contaminated
udder wash rag, milker’s
hands contaminated milking
equipment , and improperly
functioning equipment
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
Major Means of Spread
Mastitis Control
Non-ag Streps
Environment of cow
Environment of the cow by;
wet dirty lots, contaminated
bedding, milking wet cows,
poor cow prep, milking
machine air slips
Improve stall and lots
sanitation; milk clean dry
cows, avoid air leaks and
liner slips, changes bedding
frequently. Keep cows
standing after milking.
Coliforms
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.
Improve stall and lots
sanitation; milk clean dry
cows, avoid air leaks and
liner slips, changes bedding
frequently. Keep cows
standing after milking.
Staph species
Environment of cow
Poor teat dip coverage,
poor cow prep, old
bedding.
Consistent teat dipping,
adequate cow prep, and
more frequent bedding
change.
Good Milking Procedures
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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 Herd Handling
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Problem Solving Techniques
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One or more specialists: vet, fieldman, extension
agent or milking machine dealer
A visual inspection of the general environment
Good detectives
Specific approach
Problem Herd Handling
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High Incidence of Clinical Mastitis and High SCC
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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.
Problem Herd Handling

(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.
Problem Herd Handling

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
Mastitis Prevention Principles

1. Milk cow with clean, dry teats and teat
ends.


2. Prevent transfer of pathogens from cow to
cow during milking.


Impact: Milk quality, environmental mastitis, liner
slips, milk out and parlor throughput
Impact: Contagious mastitis, milk quality
3. Prevent injury to the teats during milking.

Impact: Mastitis, milk out, parlor throughput
Mastitis Prevention Principles

4. Provide an environment that allows the
cows to remain clean between milking.


5. Early detection of new infections (clinical
and subclinical).


Impact: Environmental mastitis, milk quality,
parlor throughput, cow comfort
Impact: Response to treatment, chronic
infections, culling
6. Proper use of medications.

Impact: Success of treatment, cost control,
residues in milk and meat
Mastitis Prevention Principles

7. Control duration of infections.


8. Monitor mastitis status.


Impact: Prevent outbreaks, culling information
9. Raise mastitis free replacements.


Impact: Decreased prevalence, decreased culling
Impact: Permit culling for production, reduced
herd prevalence
10. Assume all purchased replacements are
infected.

Impact: Control introduction of new pathogens
Mastitis Prevention Principles

11. Provide adequate nutrition to preclude increased
susceptibility to mastitis.


12. Fly control.


Impact: Teat end injury, new infection rate
13. Provide routine milker training


Impact: Control new infection rate
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