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