BOVINE MASTITIS: AN UPDATE

By Dr S.V. Singh, Assistant professor, Deptt. of Vet. Clinical Medicine College of Veterinary Sciences N.D.U.A. & T.

MASTITIS
 Inflammation of mammary gland parenchyma  Characterised by: abnormalities of milk & abnormalities of udder

Development of mastitis
A B

Organisms remain on .the udder surface.

Organisms enter teat canal and disrupt the teat canal barrier.

C

D

Organisms move further and affect the udder immune barrier.

Organisms establish and multiply in the udder.

Somatic cells engulfing bacteria Inflammation and damage to the udder .

PREDISPOSING Interaction of bacterial. host and environmental factors leading to mastitis FACTORS  Bacterial Factor  Host Factor  Environmental factor .

 Ability to resist phagocytosis and antibacterial substances in udder. For example. including resistance to antibiotics.  Ability to adhere to mammary epithelium and not be flushed out with the milk flow  The degree of invasiveness. . streptococci cause little pathological change to secretory cells but staphylococci initiate degenerative changes.Bacterial Factors  Ability to survive in the immediate environment of the animal  Ability to colonise the teat duct.

especially after four lactations. sphincter tone. .  Stage of lactation: more susceptible just after calving and for the following 2 months.  Presence of lesions on the teats that may predispose to inadequate milking or may harbour mastitis producing bacteria.teat shape. (Pendulous udder)  Age: older cows. anatomy of the teat canal and susceptibility to weakening of suspensory ligament.Host Factors  Genetic predisposition to mastitis .

 Milking shed environment including poor milking techniques and hygiene. .  Milking machine malfunction or inadequate design. middy approaches to the milking shed or with cause. For example. the sucking of large vigorous lambs.Environmental factors  Presence of large numbers of potential pathogens in the immediate environment of the animal. ‘Coliform’ mastitis is much more frequent in housed cattle. (poor hygiene )  General management of animals.  External traumas such as that arising from rough.

CLASSIFICATION      Per acute Acute Sub-acute Chronic Subclinical .

anorexia. depression. but systemic reaction is not so marked. . Peracute form: hot.fever. systemic disturbance . swollen and painful quarter. weakness and a rapid weak pulse  Acute form: severe inflammation. abnormal milk.

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 Chronic from: Absence of systemic signs. very few external signs of change in the udder. . positive in laboratory. recurrent episodes of mild inflammation and slight change in milk. milk appears normal unless tested.  Subclinical form: No visible abnormality in udder and milk .

cold and painful with honey like discharge from fissures  Sloughing off .Gangrenous mastitis  Cracked skin of teats/udder  Reddish to bluish black discoloration  Hard.

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Gangrenous mastitis in goat  Sloughed off teat .

Udder abscess .

Udder edema .

2. .DIAGNOSIS  STEPS INVOLVED 1.Thorough examination of udder. Examination of individual quarters 3. Examination of milk.

 Palpation.  Inspection of the udder secretion .EXAMINATION OF UDDER  Inspection.

INSPECTION
 The size and shape of the udder, individual quarters and the teats should be inspected by viewing it from front, on each side, and from behind.  Preferably the udder should be examined from the back with hind legs held apart and tail lifted upwards. This position allows view of whole udder.

PALPATION
 The teat: Palpated with the finger tips,  The quarters: Palpated (preferably after milking) with the flat of the hand, first feeling the surface, then the deeper tissue.  A convenient procedure is to start at the tip of the teat and proceed upwards.

 The teat (streak canal) normally feels firm when rolled between the fingers and all four teats should feel the same.  Abnormalities include swelling, injury and neoplasia of the tip and teat canal: also abnormal tenderness and increased warmth.  Patency of the teat canal is tested by drawing off a few streams of milk (into a stripping cup-not onto the ground).

The skin of milked out udder should be more so elastic that a fold can be pulled out. cold in gangrenous mastitis). Udder skin is palpated for  Surface temperature (exceptionally warm in mastitis accompanied by cellulitis.  Tenderness.  Thickening. .  Hardening and  Elasticity.

(i) The detection of alteration in milk as a consequence of pathophysiological changes due to an inflammatory response and (ii) The direct detection of microorganisms in milk by culture.EXAMINATION MILK OF THE Broadly classified under two categories i. .e.

individually. storage and  Storage.Sample transport collection.Sterilized glass or plastic tubes of 10-15 ml capacity with appropriate tight fitting caps  Udder .washed properly & dried with the help of a muslin cloth.  Collection -just prior to the milking particularly from the fore milk which contains more mastitis organisms.  Herd testing :a composite sample from all the quarters.  Sampling. .

.gloved.  Hands.  If stored for 15-30 minutes it should be stored at 4-5C.scrubbed thoroughly within a cotton ball soaked in 70% alcohol. from proceeding to another animal. rinsed in a germicidal solution and thoroughly dried or change the gloves after taking the sample.  Transport to laboratory .in ice. Teats .  Examinationimmediately after the collection.

Strip cup test  Routine examination of the milk using a filter cup  Moak firstly made use of strip cup test for the detection of visible particles of milk  Types of strip cups (Two)  Fine screen type : Filters the pus. NOTE: Milk that is hotter than normal may be a good indication of a Staphylococcus aureus infection . clots and flakes.  Black background type: Helps to detect the change in colour as well as presence of particles.

(1971)  Principle: reagents cause rupture of somatic cells and release cellular proteins. Mastitis (CMT) Test . These proteins unite with the reagent causing it to precipitate.California  Method described by Schalm et al. it is most likely to give the above reaction. The reaction is best seen in alkaline pH and since pH of the mastitic milk is mostly alkaline. The reagent Bromocresol purple imparts purple colour to the mixture. therefore. including the DNA.

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01 gm Sodium hydroxide – 1.5 ml Distilled water –100 ml .CMT Reagent The test reagent maybe prepared as follows Bromocresol purple – 0.5 gm Teepol – 0.

 2-3 ml of milk + equal amount of CMT reagent gentle circular motion Positive reaction : gel formation & change of colour  When the mixture is distinctly deep purple colour : + (Alkaline milk) .

(Negative) T (Trace) A distinct precipitate without gel 1+ formation and slight purplish colour positive) Viscosity of milk increased with moderate gel formation Immediate thick gel formation. INTERPRETATION Reaction No precipitate or colour change Slight precipitate Degree of test . sticking at the bottom (Weak 2+ (Positive) 3+ (Strong positive) .

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The nucleic acid forms a sodium salt in the presence of sodium hydroxide.Whiteside Test (WST)  Based on the reaction between 4% sodium hydroxide and milk.  The leukocytes of mastitic milk gets disintegrated upon contact with sodium hydroxide. producing a gelatinous mass to which serum solids and fat globules become adsorbed to produce characteristic precipitate.  Procedure: Five drops of milk + 2 drops of reagent (Stirring for about 20 seconds ) .

thread-like whorls A tenacious mass forms immediately adhering to the stick. opaque material 1+ 2+ 3+ A tenacious coagulum with little or no tendency to break down into whey and particulate material 4+ . on continued stirring the mixture separate into milky whey and white particles Thickening. the coagulum follows the stick and finally separated into a clear whey and white. the mass separates into whey and thready. clumped.REACTION Mixture remain opaque & free of particles No apparent reaction during stirring.(negative)  Thickening during stirring with little or no tendency for the mass to adhere to the stick. inspection reveals finely dispersed particles close DEGREE OF TEST .

Mastrip Test (MST)  Cellulose based bromothymol blue strip impregnated with stabilized ion  One drop of milk is placed on the mastrip  The colour reaction is graded as Reaction Degree of test No change in colour (yellow) Light green + Dark green ++ Bluish green +++ .

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Electrical Conductivity  The electrical conductivity of milk increases in mastitis owing to altered concentration of ions in mastitic milk.  The electrical conductivity of normal milk ranges between 4. .  Measured by using electrical conductivity meter.  Conductivity is measured in Siemens (S) and is calculated by dividing amphere by voltage.5 mS/cm.0 – 5.

 Normal SCC in milk is generally below 200.000 per ml  An SCC above 250.000 .300.. .Somatic Cell count  Interpretations.000 is considered abnormal and nearly always is an indication of bacterial infection causing inflammation of the udder.

TREATMENT Antibiotics Systemic Intramammary Preferably the same antibiotic should be used Anti inflammatory drugs Anti histamines .

plasma ratio.Antibiotic therapy  Mastitis is the most common reason for antibiotic use in the dairy industry  Properties of antibiotic therapy intended for mastitis therapy  The bioavailability from intravenous administration with low plasma protein binding and high milk. .  The antibiotic should have low minimum effective concentration (MEC) against major causative pathogens with longer elimination half-life from the udder tissue.

ampicillin & cloxacillin and third generation cephalosporins Best performance: Ampicillin. Framycetin. Drugs of choice Aminoglycosides neomycin. Erythromycin & Tylosin Medium performance: Penicillin G. Cloxacillin & Tetracyclines Poor diffusers which do have a longer T1/2 : Streptomycin & Neomycin . Amoxycillin.

2004 Sharma.Trial reports (gangrenous mastitis) Treatment group Ceftriaxone Ceftriaxone % efficacy 66.6 93.2008 Ceftriaxone + gentamicin Ceftriaxone + gentamicin 92 83. 2004 Singh et al . 2004 Singha et al.75 Reference Singh.33 .

 The bacteria too sometimes become refractory to the effects of the drug.Failure therapy of antibiotic  Development of resistance:  indiscriminate use of antibiotics  the ubiquitous nature of mastitogens. .

 The inflammation. . edema or fibrosis of the mammary gland results in a poor distribution of the drug within the udder.Demerits of intramammary therapy  Makes animal susceptible to the injury to teat canal  if sterile conditionsplaces microbes directly into the udder  Causes the dilation of teat canal lumen. and enhancing bacterial penetration.

ALTERNATE THERAPY      ANTIOXIDANT THERAPY PHYTOTHERAPY HOMEOPATHY CYTOKINE THERAPY OXYTOCIN THERAPY .

Entry of bacteria into mammary gland Mobilisation of PMN cells Engulf and kill bacteria through RESPIRATORY BURST Release of free radicals Adequate antioxidant Insufficient antioxidant Allow a more active and more prolonged effect of a cow’s natural immune system on invading bacteria Free radicals accumulate OXIDATIVE STRESS .

 When ROS are not effectively and safely removed. but they are not 100% effective. mastitis being one of them . oxidative stress may impair health in dairy cows both directly and indirectly  Directly: per oxidative damage to important lipids and macromolecules  Indirectly: by changes induced in cellular membranes and components  Tissue injury contributes to the development of disease conditions. Cells can tolerate a mild oxidative stress  Antioxidants.scavange and minimize the formation of ROS.

Commonly used antioxidants      Vitamin E Vitamin A Vitamin C Selenium Zinc .

 Plays a regulatory role in the biosynthesis of various inflammatory mediators and influences both cellular and humoral immunity.  An integral component of all lipid membranes and protects lipid membranes from attack by Reactive Oxygen Species.. ROS.1993) .  Increases intracellular killing of both Staphylococcus aureus and Escherchia coli (Hogan et al.VitaminE Supplementation  Most important lipid soluble antioxidant.

and first two to three weeks of lactation  Large quantity of the vitamin E is secreted in the colostrum causing a 47% drop in maternal Vitamin E concentration  Increased cortisol concentration in the blood prior to calving reduces vitamin E content in neutrophils.Vit E conc. the time of maximum susceptibility. Vitamin levels are lowest around calving.  Therefore. . during periparturient period  Declines around 7 to 10 days prior to calving.

12.25% incidence  Singh et al.5% incidence  Unsupplemented group -56. (2000)  80% efficacy in animals administered Vitamin E and Selenium injections (E care Se) and gentamicin  60% efficacy in gentamicin treated group. Nauriyal (1996)  Dose: 1000 IU of tocopherol during the dry period and during early lactation  Result:  Supplemented group . .

Dose recommendations  Dry cows :1000 IU/day  Lactating cows :500 IU/day Injection of selenium and vitamin E or feeding supplemental amounts of these nutrients during the 3 weeks prepartum may reduce the incidence of post lactational disorders. .

1998 Pachauri et al. 1996..PHYTOTHERAPY Ingredients/ Product Findings References in Saxena et al.) treatment prophylaxis SCM Bonmilk 100% recovery 79. 1999 Dash.. 2001 Mastilep (Dabur Efficacious Ayurvet Ltd.88% Ocimum sanctum with Azaderachta Aqueous extract of 100% recovery Tinospora cordifolia .55% cure rate Oil extract of 88... and Madan et al. of Kamal et al. 1995.

 The immunopotentiating activity of these drugs enhance the body’s defence mechanism along with udder immunity. . antiinflammatory.Advantages  Nontoxic nature  Cost effectiveness  The ingredients have antibacterial. analgesic and immunostimulatory properties  Effective against not any specific organism but plethora of organisms.

4 doses. Animal is often Iying down. 4 doses. Udder very hot and red. Pain less intense when pressed. and pulse is quick and strong. Also useful for summer mastitis cases with purulent abscess. Animal is hot. fever and putrified curd like appearance of milk .  Phytolacca 30 c : Clinical cases with sour. 3 doses a day for 3 days.  Silicea 200 c : Few flakes in thin yellow milk. Chronic cases: 1 dose 2 times a week for one month. 1 dose every hour. coagulated milk.  Ipeca 30 c : Useful for treating internal bleeding that produces pink or bloody milk. 2 doses a week for 4 weeks. hard.HOMEOPATHY Belladonna 1 m: For acute postpartum mastitis. Especially good for chronic cases with fibrosis.  Calcaria florica with silicia: Chronic mastitis and fibrosis. painful to the touch. Bryonia Alba 30 c : udder swollen. Chronic cases with small clots at mid-lactation.  Lachesis: Udder discoloration. Acute cases: 1 dose every 4 hours.

restrict the contact of populations of environmental bacteria with the mammary gland.  Good hygiene .break the chain of transmission  Eliminating the source of infection (the infected mammary gland.  Environmental mastitis . by isolation and quarantine) and  With strict sanitation at the time of milking.PREVENTION & CONTROL  Contagious mastitis .

10 min (prevents the contact of microbes to udder). Invasion state :  Avoid the animals to sit immediately after calving.  Teat dipping  Infection stage :  Boosting udder immunity by supplementing different antioxidants  Inflammation stage :  immediate medical care  animals should be segregated from the rest. approx. .

Desh Deepak Singh. Harnam Singh .Satyavrat Singh. Sonu Jaiswal.