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Bovine Mastitis
Sukolrat Boonyayatra
DVM, MS
Clinic for Ruminants
What’s mastitis ?
Inflammation of one or more quarters of
the udder
Normal Inflamed
Swelling pain warm redness
Mammae = breast -itis = Latin suffix for
inflammation
Causes
Intramammary Infection (IMI): Bacterial infection Mycoplasmal infection Mycotic (fungal) infection Algal infection
Mechanical trauma Predisposes Thermal trauma the gland to IMI Chemical insult
Economic Losses 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
Determinants of Mastitis
Timing of infection and stage of lactation Active involution
High Pressure in the gland Bacteria inside the gland Teat dipping ceases. Phagocytic efficiency Increasing of immunoglobulins and lactoferrin cannot overri
de the problems noted above. Dry cow treatment can not reduce coliform IMI during active
involution. Reducing the period of active involution by infusing colchici
ne (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 tim
e are not effective in preventing new IMI. IgG1 is not normally an effective opsonin in the mammary g
land. Antibiotic concentration Teat dipping
Timing of infection and stage of lactation
Early lactation Metabolically stressed Mastitis is sometimes associated with high conce
ntrate feeding which accompanies early lactation.
Timing of infection and stage of lactation
Nutrition and MastitisMicronutrient 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 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
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.
Mastitis Clinical Syndromes
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
Mastitis Clinical Syndromes
Abnormal Milk
Abnormal Udder
Somatic Cell Count
~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
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)Lactose (good) Total proteins (good)Total proteins (good) Casein (good)Casein (good) Immunoglobulins (bad)Immunoglobulins (bad) Solids not fat (good)Solids not fat (good) Total solids (good)Total solids (good) Fat (good)Fat (good) Lipase (bad)Lipase (bad) Sodium (bad)Sodium (bad) Chloride (bad)Chloride (bad) Calcium (good)Calcium (good) Phosphorus (good)Phosphorus (good) Potassium (good)Potassium (good) Trace minerals (bad)Trace minerals (bad) Cheese (good)Cheese (good)
Heat stability (good)Heat stability (good)
Lactose (good)Lactose (good) Total proteins (good)Total proteins (good) Casein (good)Casein (good) Immunoglobulins (bad)Immunoglobulins (bad) Solids not fat (good)Solids not fat (good) Total solids (good)Total solids (good) Fat (good)Fat (good) Lipase (bad)Lipase (bad) Sodium (bad)Sodium (bad) Chloride (bad)Chloride (bad) Calcium (good)Calcium (good) Phosphorus (good)Phosphorus (good) Potassium (good)Potassium (good) Trace minerals (bad)Trace minerals (bad) Cheese (good)Cheese (good)
Heat stability (good)Heat stability (good)
Decreased 5 to 20%Decreased 5 to 20% Decreased slightlyDecreased slightly Decreased 6-18%Decreased 6-18% IncreasedIncreased Decreased up to 8%Decreased up to 8% Decreased 3 t0 12%Decreased 3 t0 12% Decreased 5 to 12%Decreased 5 to 12% Increased rancidityIncreased rancidity IncreasedIncreased IncreasedIncreased DecreasedDecreased DecreasedDecreased DecreasedDecreased Slight increaseSlight increase Decreased curd strength, fat Decreased curd strength, fat
and yieldand yield Reduced Reduced
Decreased 5 to 20%Decreased 5 to 20% Decreased slightlyDecreased slightly Decreased 6-18%Decreased 6-18% IncreasedIncreased Decreased up to 8%Decreased up to 8% Decreased 3 t0 12%Decreased 3 t0 12% Decreased 5 to 12%Decreased 5 to 12% Increased rancidityIncreased rancidity IncreasedIncreased IncreasedIncreased DecreasedDecreased DecreasedDecreased DecreasedDecreased Slight increaseSlight increase Decreased curd strength, fat Decreased curd strength, fat
and yieldand yield Reduced Reduced
What are the health concerns of mastitis ?
Animal health Loss of functional quarter Lowered milk production Death of cow
Human health Poor quality milk antibiotic residues in milk
How severe can mastitis be ?
Subclinical Mastitis ~ 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 cas
es Inflamed udder Clumps and clots in milk
Acute type major type of clinical mastiti
s bad milk loss of appetite depression
prompt attention needed Chronic type bad milk cow appears healthy
What causes mastitis ?
Bacteria ( ~ 70%) Yeasts and molds ( ~ 2%)
Unknown ( ~ 28%) physical trauma weather extremes
Where do these organisms come from ?
Infected udder Environment bedding soil water
manure Replacement animals
How does mastitis develop ?
Cow 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 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
Bacterial Infection: Streptococci 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
Bacterial Infection: Staphylococci 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 monon
uclear 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 ductsThe lesions affected the intralobular duct, intralobular duts and alveoli (Azan x 30).
Bacterial clumps(arrows)surrounded by alveolar epithelial cells undergoing necrosisThrombus(*)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
Bacterial Infection: Coliforms
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
Bacterial Infection: Other organisms
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
Bacterial Infection: Other organisms
How is mastitis diagnosed ?
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
Treatment
Clinical mastitis Strip quarter every 2 hours Oxytocin valuable high temp, give NSAIDs Seek veterinary assistance
Treatment with penicillins Subclinical mastitis Questionable
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Standardized Milking Procedures Stanchion/ Tie stall
Ware gloves Wipe off excess dry manure
, straw and bedding Strip each teat into a stripcu
p 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 stripcu
p Dip teats with an approved
pre-dip Dip 3-4 cows Allow the pre-dip to react for
at least 30 sec.
Stanchion/ Tiestall Clean teat and teat ends usi
ng single paper towel or 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
Parlor Return to the first cow and c
lean teat and teat ends using a single paper towel or 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
Standardized Milking Procedures
Visualization and palpation of the udderVisualization and palpation of the udder
Detection of Somatic CellsDetection of Somatic CellsCalifornia Mastitis TestCalifornia Mastitis Test
Detection of Mastitis Detection of Mastitis
N-acetyl-ß-D-glucosaminidase N-acetyl-ß-D-glucosaminidase (NAGase)(NAGase) - a lysosomal enzyme which increases in milk - a lysosomal enzyme which increases in milk when mastitis is present when mastitis is present
Indirect chemical tests to detect mastitis 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) 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 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
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.
CMT CMT scorescore
InterpretationInterpretation Visible reactionVisible reaction Total cell count Total cell count (/ml)(/ml)
00 NegativeNegative Milk fluid and normalMilk fluid and normal 0-200,0000-200,000
0-25% neutrophils0-25% neutrophils
TT TraceTrace Slight precipitationSlight precipitation 150,000-500,000150,000-500,000
30-40% neutrophils30-40% neutrophils
11 Weak positiveWeak positive Distinct precipitation but no Distinct precipitation but no gel formationgel formation
400,000-1,500,000400,000-1,500,000
40-60% neutrophils40-60% neutrophils
22 Distinct Distinct positivepositive
Mixture thickens with a gel Mixture thickens with a gel formationformation
800,000-5,000,000800,000-5,000,000
60-70% neutrophils60-70% neutrophils
33 Strong positiveStrong positive Viscosity greatly increased. Viscosity greatly increased. Strong gel that is cohesive Strong gel that is cohesive with a convex surface.with a convex surface.
>5,000,000>5,000,000
70-80% neutrophils70-80% neutrophils
Correlation between the California mastitis test result and the somatic cell count.
Steps involved in employing HAC- CP based concepts for establishin
g proper milking procedures 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, fa
cilitator) 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 stan
dardized 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.
Factors Affecting Somatic Cell Counts 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 1. Milk Culture and Sensitivity Testing 2. Treatment During Lactation 3. Drying Cows Off Early 4. Culling
1. Milk Culture and Sensitivity Testing High SCC >500,000 cells/ml Very useful when:
High SCC two or more tests Beginning of lactation
2. Treatment During Lactation Strep. agalactiae infection Very few cases of subclinical mastitis High SCC vs culture vs sensitivity
3. Drying Cows Off Early
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
Persistently high SCC from lactation to lactation
Staph. aureus or Mycoplasma spp. Milk production
5. Milking Routine
High SCC cow could be milked last or the milking machines could be sanitized after milking.
Mastitis Bulk Tank Culture Report Interpretation
Type of BacteriaType of Bacteria Usual Infection Usual Infection CauseCause
Major Means of SpreadMajor Means of Spread Mastitis ControlMastitis 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.
Type of BacteriaType of Bacteria Usual Infection Usual Infection CauseCause
Major Means of SpreadMajor Means of Spread Mastitis ControlMastitis 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.
Mastitis Bulk Tank Culture Report Interpretation
Good Milking Procedures 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
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.
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
Problem Herd Handling
Mastitis Prevention Principles 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, parlo
r throughput, cow comfort 5. Early detection of new infections (clinical a
nd subclinical). 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. 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 her
d prevalence 10. Assume all purchased replacements are i
nfected. Impact: Control introduction of new pathogens
Mastitis Prevention Principles
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 co
mpliance
Mastitis Prevention Principles