MASTITISCAREINTRODUCTIONIt is a formulation effective in controlling mastitis in sub-clinicalform and also it can be used as an adjunct in mastitis therapyMastitis, an inflammatory response of the mammary gland causedusually by bacteria, is probably the most costly of the infectious,endemic diseases to affect dairy cows and other dairy species. Itsimpact is on animal production, animal welfare and the quality ofthe milk produced.EFFECTS ON MILK COMPOSITIONMastitis can cause a decline in potassium and lactoferrin. It alsoresults in decreased casein, the major protein in milk. As mostcalcium in milk is associated with casein, the disruption of caseinsynthesis contributes to lowered calcium in milk. The milk proteincontinues to undergo further deterioration during processing andstorage. Milk from cows with mastitis also has a higher somaticcell count. Generally speaking, the higher the somatic cell count,the lower the milk quality.SIGNS AND SYMPTOMS:A wide range of differing symptoms will be shown with differenttypes of infection. Milk may become watery or thickened or pus-like, and may contain clots which vary in color from yellow toblood clots. The clots may also vary considerably in character. Insome infections they are large, slimy clots. Other clots may bepurulent; some infections produce mealy or flaky clots. Some clotsmay consist of fine flocculation that is seen like small pieces ofblotting paper. The nature of the milk may be changed in all sortsof ways. Thus, on some occasions, it is merely thinner and paler. Itmay be thickened and amber in color, darkened, or blood stained,and have varying degrees of unpleasant smell. Milk productionmay be decreased or ceased altogether and be replaced by pus,clots or watery material. The condition of the udder may becomehot, tense, and painful and later develop fibrotic changes withhard lumps, or it may be shriveled and wasted. In some severetypes, one or more quarters of udder may die and slough right offleaving a filthy, gaping wound. In severe cases the animals will
show general symptoms of toxemia or septicemia, being off theirfeed, shivering and scouring and may die.(http://www.pakissan.com/english/allabout/livestock/mastitis.monster.threat.to.dairy.industry.shtml)CAUSANTS:These include contagious pathogens, environmental bacteria,opportunistic bacteria and other organisms that less frequentlycause mastitis less frequently.It would appear that as contagious pathogens were reduced,opportunistic and environmental pathogens seemed to play agreater role in causing persistent infections. 1. Brucella melitensis 2. Corynebacterium bovis 3. Enterobacter aerogenes 4. Escherichia coli, (E. coli) 5. Klebsiella oxytoca 6. Klebsiella pneumoniae 7. Mycoplasma (various species) 8. Pasteurella spp 9. Proteus spp 10. Prototheca wickerhamii (achlorophyllic algae) 11. Prototheca zopfii (achlorophyllic algae) 12. Pseudomonas aeruginosa 13. Staphylococcus aureus 14. Staphylococcus epidermidis 15. Streptococcus agalactiae 16. Streptococcus uberis 17. Trueperella pyogenes (previously Arcanobacterium pyogenes) Causes of clinical mastitis in the Institute for Animal Health dairy herd (% positive identifications) 1964 1985–90 2000 Streptococcus agalactiae 1·9 0 0 Streptococcus 22 8·3 0 dysgalactiae Streptococcus uberis 20 43 33 Staphylococcus aureus 43 20·3 16 Coliforms 2·4 22·8 43 Arcanobacterium 4·5 5·4 1·2 pyogenes
(http://www.scielo.br/scielo.php?pid=S1517-83822010000300003&script=sci_arttext)Cost of an average case of clinical mastitis in a dairy cow producing 7000 kg milk per lactation (from Berry et al. 2004)Factor Cost (£)Labour, 2 h at £6 12Treatment, drugs and vet 11·3Discarded milk 26Production loss (10%) 135
Cost of an average case of clinical mastitis in a dairy cow producing 7000 kg milk per lactation (from Berry et al. 2004)Factor Cost (£)Reduced food intake −56·25Fatality (1%) 3Total 131PREVENTIONNational Mastitis Council Recommended Milking Procedures Provide a clean, stress-free environment for cows. A clean environment is essential to preventing environmentally caused mastitis. For maximum production, cows should have minimum stress. Stress reduces the milk letdown process. Handle cows calmly. Check foremilk and udder for mastitis. Examine the udder for swelling, heat or pain, and, using a strip cup or plate, examine the foremilk from each quarter prior to every milking. Wash teats with an udder wash sanitizing solution. Washing each teat aids milk letdown and removes mud, dirt, manure and other foreign objects on the skin. Dry teats completely with individual paper towels. Milking machines are designed to stay securely attached to a dry teat. Drying the teat also prevents possible contamination of the milk and teat by bacteria in the water running off the cow’s udder and teats. This water, if present, acts as a freeway for bacteria to enter the milking system. Remember, the goal of every mastitis-control program is to prevent the introduction of bacteria into a normal and healthy mammary gland. Attach the milking unit within one minute after the start of stimulation. The milk letdown process that follows the release of oxytocin after udder stimulation is highest for three to five minutes. Thus, using this physiologic event to its maximum for the most efficient removal of the milk is important.(http://www.ag.ndsu.edu/pubs/ansci/dairy/as1126.pdf)CONVENTIONAL TREATMENTConventional treatment is to use antibiotic therapy, althoughalternatives including herbal and homoeopathic approachesassume some importance.The use of antibiotics to treat mastitis is contentious in itself withthe methods varying internationally. Australasia, the USA and theUK amongst others, treat mastitis by intramammary inoculation ofan antibiotic-containing paste, using one syringe every one or twomilkings for up to 3 days. Others, principally in Nordic countries,use intramuscular injection as the preferred route of treatment.The intramammary preparations are usually multicomponentincluding more than one antibiotic and often a corticosteroid to
treat inflammation. The intramuscular products are usually singleactive products, often simply penicillin G. Arguments exist on theformulation and the pharmacodynamics to reach the site ofinfection, a problem with an organ that is relatively dense andweighs several kilograms.Ziv (1980) showed that approximately 97% of intramammaryproduct stays in the udder and is void in milk whilst systemictreatment results in only 3% product becoming intramammarywith the rest void mostly in urine, after systemic dispersal. Thebasic argument weighs use of nonspecific and broad spectrumintramammary treatment against simple products, nontargetedand used in significantly greater amounts. It would also appearthat there might be good reasons to use more treatment thanrecommended on the label of the products.(http://onlinelibrary.wiley.com/doi/10.1111/j.1365-2672.2005.02649.x/full)EFFICACY OF DRUG DELIVERYThe administration of drugs can be done either directly into theteat canal, as previously described for dry cow therapy, in the formof intramammary infusions, but can also be given parenterally byintravenous or intramuscular injection (65). The route of choicefor subclinical mastitis is usually by intramammary infusion; and inthe case of severe acute clinical mastitis, a combination ofparenteral and intramammary treatment is usually necessary(104).To be effective, the drug has to exert specific antimicrobial activityat the site of infection (34) and must have certain characteristics tobe an effective agent in the mammary tissue. The pH of bloodplasma is 7.4. The pH of milk varies between 6.4 and 6.6, butincreases to 7.4 in the case of an infection. Most antibiotics areweak organic acids or bases and exist in both an ionised and non-ionised form in varying proportions in blood and milk, dependingon the change in pH of the environment. Drugs that areadministered parenterally must pass from the circulatory bloodsystem and into the milk and milk tissue via lipid membranes. Theactive fraction of the drug must be in a non-ionised, non-proteinbound, lipid-soluble form to pass this blood-to-milk barrier (104).Antibiotics that are administered via the teat opening must reachthe site of infection in the teat canal or upper cistern, but often thedistribution is uneven and diffusion through the mammary ductswhere severe inflammation and swelling is present may block themovement of the therapeutic agent (24). Added to this, mostpathogens have the ability to invade the epithelium tissue. In thecase of S. aureus infection, interaction with antibiotics is preventedby the formation of fibrous scar tissue. The scar tissue may alsohave no blood supply, rendering intramuscular or intravenous drug
therapy less effective (65). Some bacteria may also evadeinteractions with antibiotics once engulfed by macrophages, wherethey remain active within the leukocyte and can cause recurrentinfections once the antibiotic has been eliminated from the area(65). The formation of biofilms within the teat canal as bacteriaadhere to bacteria on the epithelium surface may also contributeto the ineffectiveness of local intramammary infusions (52).(http://www.scielo.br/scielo.php?pid=S1517-83822010000300003&script=sci_arttext)NEED FOR ALTERNATIVES TO ANTIBIOTICS:A strong drive by many Governments towards reducing antibioticresidues in animal food products has necessitated and establishedthe need in finding alternatives to antimicrobial agents.PROTOCOLS SUGGESTED:Milk from the infected quarters is to be cultured to determine thetype of micro-organism causing the infection; before startingtreatment.After treatment also milk can be subjected to plating to see thepresence or absence of the pathogens causing clinical mastitis.Milk samples showing 3 + CMT reactions with SSC (>2,700,000 cellsper ml) but no visible abnormality of milk or udder, and milksamples with SSC≥2,700,000 cells per ml with visible abnormalityof milk or udder were classified as subclinical and clinical mastitis,respectively(Radostits et al., 1994).CITATIONS:The use of L. fermentum CECT5716 or L. salivarius CECT5713appears to be an efficient alternative to the use of commonlyprescribed antibiotics for the treatment of infectious mastitisduring lactation.(http://cid.oxfordjournals.org/content/50/12/1551.full)Improving host defences can result in rapid elimination of newinfections. Supplementing of selenium and vitamin E andimproving general nutrition during high-risk periods such asperiparturient and drying-off periods can increase host defencemechanisms.(http://www.scielo.br/scielo.php?pid=S1517-83822010000300003&script=sci_arttext)Sears et al. investigated the use of a nisin-containing germicidalformulation in preventing mastitis in cattle.
(Sears, P.M.; Smith, B.S.; Stewart, W.K.; Gonazalez, R.N. (1992).Evaluation of a Nisin-based Germicidal Formulation on Teat Skin ofLive Cows. J. Dairy Sci., 75: 3185-3190.)Steffert (1993) and, Antila and Antila (1979) reported decreasedascorbic acid concentration in milk of mastitis dairy cows.Contents:Propreitory blend of Minerals like Selenium, Nisin producing L.lactis, Lacticin producing L. lactis, Amino acids like Valine andLysine, Organic acids like Tartaric acid, vitamins like Ascorbic acidand E, and Probiotics like L. fermentum and L. salivariusContra indications: NoneSide effects: NoneDosageCurative:50gm for 4 days as electuary per animal1-2 g/ animal in water as paste externally applied to the udder,teats and surrounding parts and the ground where that cattle liedown, preferably by spray thrice a dayWithdrawal times: NonePackaging: 200gmx50REFERENCES: Smith, K.L., Hillerton, J.E. and Harmon, R.J. (2001) National Mastitis Council Guidelines on Normal and Abnormal Milk based on Somatic Cell Counts and Signs of Clinical Mastitis. Madison, WI, USA: National Mastitis Council, 3 pp. Stableforth, A.W., Hulse, E.C., Wilson, C.D., Chodhowski, A. and Stuart, P. (1949) Herd eradication of S. agalactiae by simultaneous treatment of all cows with five doses of 100 000 units of penicillin at daily intervals and disinfection. Vet Rec 61, 357 – 362. Teale, C.J. and David, G. (1999) Antibiotic Resistance in Mastitis Bacteria. Proceedings of the British Mastitis Conference, Institute for Animal Health, pp. 24 – 29. Watts, J.L. (1988) Etiological agents of bovine mastitis. Vet Microbiol 16, 41 – 66. Ziv, G. (1980) Drug selection and use in mastitis: systemic versus local therapy. J Am Vet Med Assoc 176, 1109 – 1128.