MANAGEMENT OF MASTITIS WITH APPLICATION OF ETHNOVEVETERINARY AND OTHER THERAPIES IN DAIRY ANIMALS

MANAGEMENT OF MASTITIS WITH APPLICATION OF ETHNOVEVETERINARY AND OTHER THERAPIES IN DAIRY ANIMALS

K.P. Singh*¹ and Praneeta Singh²

Government Veterinary Hospital, Deoranian, Bareilly,

Department of Animal Husbandry, Uttar Pradesh, India

1: Veterinary Officer, Government Veterinary Hospital, Deoranian, Bareilly, Uttar Pradesh Email: drkpsvet@rediffmail.com

2: Assistant Professor, Department of Livestock Products Technology, C.V.A.Sc., GBPUAT, Pantnagar, U.S.Nagar, Uttrakhand Email: vet_praneeta12@rediffmail.com

*Corresponding Author: Veterinary Officer, Government Veterinary Hospital, Deoranian, Bareilly, Uttar Pradesh Email: drkpsvet@rediffmail.com

 

Abstract

Mastitis is globally considered the most expensive disease of dairy animals caused by plethora of organisms. Though it is difficult, rather impossible, to eradicate the disease, but the development can be checked by adopting certain prevention techniques like dry cow therapy, phyto therapy, teat sealants, teat dips, cytokines, antioxidant therapy etc. The clinically affected animals should be provided prompt treatment and should be milked at last with proper disposal of milk. The present article describes the techniques that can be adopted to decrease the incidence of mastitis as well to prevent the development of new cases of mastitis.

Key Words: Dairy animals, Ethnoveterinary, Mastits, Therapies

 Introduction

Mastitis is an inflammation of mammary gland parenchyma, which is caused by bacteria and its toxins , characterized by physical, chemical and bacteriological changes in the milk and pathological changes in the glandular tissue of the udder. It is the most expensive disease of dairy cattle resulting in the reduction in milk production, losses in milk quality and quantity, losses due to discarded milk, premature culling, treatment costs and labour. The economic losses due to mastitis worldwide have been estimated at $35 billion (Wellenberg et al 2002). Despite an appropriate choice of antimicrobial, treatment of mastitis may be unsuccessful. Current treatments of clinical mastitis during lactation are not very successful and cure rates are poor, especially in the case of Staphylococcus aureus mastitis.

Mastitis is caused by a wide spectrum of pathogens and, epidemiologically categorized in to contagious and environmental mastitis. Contagious pathogens are those for which udders of infected cows serve as the major reservoir. They spread from cow to cow, primarily during milking, and tend to result in chronic sub-clinical infections with flare-ups of clinical episodes. Contagious pathogens include: Staphylococcus aureus, Streptococcus agalactiae, Mycoplasma spp. and Corynebacterium bovis (Radostits et al.,2007). On the other hand, environmental mastitis can be defined broadly as those intra-mammary infections caused by pathogens whose primary reservoir is the environment in which the cow lives (Smith et al.,1985). Environmental pathogens include E. coli, Klebsiella spp., Strept. dysgalactiae and Strept. uberis and the majority of infections caused by these pathogens are clinical and of short duration (Harmon et. al.,1994).

Mastitis is an outcome of an interplay of host, environment and organisms (Kinde et. al., 2015). Response of bacterial invasion of the udder depends upon pathogenicity of the bacterial species involved and competency of the cow’s immune system.  To develop a suitable prevention protocol it is advisable to study the development of mastitis that will provide avenues where we can target to prevent the development of mastitis.

Development of mastitis

Mastitis is nearly always caused by microorganisms, usually bacteria, that invade the udder, multiply in the milk-producing tissues, and produce toxins that are the immediate cause of injury Shaheen et al (2016).

The udder immune system can be viewed as a three-tiered defense starting with physical barriers and non- specific and specific immune responses. Physical barriers and non-specific immune responses comprise the innate or natural immunity. These immune responses are not antigen specific, nor do they have any memory response. Cell mediated and humoral immune responses comprise active immunity and are antigen specific and have memory.

Physical barriers of the udder are anatomic features of the teat and associated structures that pose a physical blockade to invading bacteria at the teat sphincter, the point of entry. These anatomic features include the teat skin, teat sphincter muscle and keratin plug. The teat end serves as the body’s first line of defense against infection. A smooth muscled sphincter, which surrounds the teat canal, functions to keep the teat canal closed, prevent milk from escaping, and prevents bacteria from entering the teat. The cells lining the teat canal produce keratin, a fibrous protein with lipid components (long chain fatty acids) that have bacteriostatic properties. This keratin forms a barrier against bacteria. Teat skin that has abrasions, cracks or is smugged with dirt increases bacteria colonization of the skin greatly increasing bacterial numbers around the teat sphincter and thusly increasing risk of bacterial penetration through the teat duct. Bacteria may be present near the opening of the teat canal, either through dirty and wet conditions at the teat end, through teat end lesions or colonization, on contaminated surfaces of milking units (liners or claws), or cow prep procedures. Following milking the teat duct is dilated, greatly increasing the risk of bacterial penetration. Contraction of the teat sphincter takes time, which is why providing cows fresh feed following milking is promoted. This practice allows time for the teat sphincter to constrict, closing off the teat opening, before cows return to their stalls and have direct contact with the environment. The keratin plug is produced by skin lining the teat duct. Keratin is gummy, has bacteriostatic activity and completely occludes the teat canal. Trauma to the teat renders it more susceptible to bacterial invasion, colonization, and infection because of damage to keratin or mucous membranes lining the teat sinus. The canal of a damaged teat may remain partially open. Conditions which contribute to trauma include: incorrect use of udder washes or cleaning compounds, wet teats, improper mixing or freezing of teat dips, frostbite, failure to prep cows or pre-milking stimulation for milk ejection, overmilking, and insertion of mastitis tubes or teat cannulae.

An inflammatory response is initiated when bacteria enter the mammary gland and this is the body’s second line of defense. The bacteria enter mammary glands of cows through their teat canal, where they colonize, proliferate, and release toxins, damaging the mammary gland cells (Quirk et. al.,2012). These bacteria multiply and  produce toxins, enzymes, and cell-wall components which stimulate the production of non-specific immune responses including phagocytic cells (i.e., somatic cells), inflammatory response, complement cascade and lactoferrin. Phagocytic cells of various types are by in far the most important mediator of mastitis infections. All though there are a number of cell types, neutrophils and macrophages account for the majority of phagocytic cells in mastitis infections. Polymorphonuclear neutrophil (PMN) leukocytes and phagocyctes move from bone marrow towards the invading bacteria and are attracted in large numbers by chemical messengers or chemotactic agents from damaged tissues. Masses of PMN may pass between milk producing cells into the lumen of the alveolus, thus increasing the somatic cell count (SCC) as well as damaging secretory cells. Macrophages play multiple roles in coordinating activation of the specific immune response. After engulfing a foreign antigen, macrophages will present these on their cellular surface to stimulate lymphocytes to respond.

Numbers of somatic cells remain in large concentrations after bacteria are eliminated until healing of the gland occurs. Clots formed by the aggregation of leukocytes and blood clotting factors may block small ducts and prevent complete milk removal. Damage to epithelial cells and blockage of small ducts can result in the formation of scar tissue in some cases, with a permanent loss of function of that portion of the gland. In other cases, inflammation may subside, tissue repair may occur, and function may return in that lactation or the subsequent one (Harmon, 1994). Complement proteins also move into the inflamed area and promote phagocytosis and killing of bacteria by neutrophils and macrophages. Lactoferrin is a specialize protein synthesized in the udder that binds iron making it unavailable for bacterial growth, especially coliform bacteria.

Staphylococcus aureus can survive within phagocytic cells or become walled off within mammary tissue, thus evading immune detection and preventing its elimination.

The common reasons for mastitis treatment failure associated with the drug factors are (Erskine et al 2003; Serieys et al 2005):

Improper antimicrobial selection Short half-life of the drug Inadequate local tissue concentration Side effects of the drug Other factors that will lead to inactivation of the antimicrobial in vivo or in vitro

Low bio-availability Weak passage of drug across the blood-milk barrier High degree of milk and serum protein binding Combined use of microbicidal and microbiostatic antimicrobials

 

In the best case scenario, the bacteria are cleared without subsequent colonization of mammary tissues. Successful bacterial colonization of mammary tissue can result in a wide spectrum of disease outcomes, ranging from subclinical (e.g., no obvious change to udder or milk) to peracute clinical (e.g., severe systemic disease symptoms with dramatic changes to udder and milk secretion) mastitis (NMC, 1996).

Current treatments of clinical mastitis during lactation are not very successful despite an appropriate choice of antimicrobial, treatment of mastitis may be unsuccessful (McKellar 1991). Insufficient contact of the antimicrobial with organisms at the site of infection is a major cause of mastitis treatment failure (Serieys et al 2005). Cure rates are, especially poor in the case of Staphylococcus aureus which is responsible for chronic infections and huge economic losses (Gruet et al 2001). Estimate of microbial cure rate during lactation in case of Staph aureus mastitis is usually between 25 and 50% (Sol et al 2000).

Prevention of Mastitis

Prevention of mastitis aims at strengthening these udder immune systems through proper management, boosting host’s immune response and minimizing the number of causative organisms.

Key points to minimize mastitis in dairy cows

• Environment

• Sanitization and udder hygiene

• • Udder hygiene,
  • Environmental hygiene and
  • Sanitization measures for milker’s hands or milking machines.
• Nutrition: The micronutrients being important for proper immune cell function and protection, deficiencies of these micronutrients can have serious consequences on mammary gland health and thus supplementation could provide great benefit to the control of bovine mastitis (Singh et al., 2003).

• Balanced ration
• Antioxidant therapy

• Prompt treatment
• Dry Cow Treatment
• Vaccination?

Prevention strategies can be designed based on pathogenesis of mastitis

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

Another way to prevent mastitis is to formulate strategies based on etiology as follows:

Contagious Mastitis : Contagious mastitis can be effectively controlled through a rigorous program of teat dipping and dry cow antibiotic treatment. Teats must be dipped in germicide after each milking (this decreases incidence of the disease). Each quarter must be treated with dry cow antibiotics at end of lactation (this decreases prevalence of the disease). Cows with contagious mastitis should be milked last or a separate milking claw used for the infected cows. Milking claws should be flushed with hot water or germicide after milking infected cows (called back flushing). Individual cloth/paper towels should be used to wash/dry teats. Milkers should have clean hands and wear latex gloves. New additions to the herd should be cultured and persistently infected cows should be culled. Teat lesions should be minimized (from chapping, frostbite, stepped-on teats, lacerations, or machine damage). Heifers can be given dry cow antibiotic treatment during gestation if S. aureus is a problem in the heifers.

Environmental Mastitis : Environmental pathogens are more difficult to control than the contagious pathogens. Many of these organisms are resistant to germicides in teat dip and antibiotics in dry cow therapy. Identification of the source and removal (bedding, ponds, mud) is the key to control. Udders can be clipped to minimize the amount of manure clinging to the glands. Only clean dry teats should be milked. Teats should be pre-dipped with germicide before milking. Cows should be kept standing after milking (offer them feed). Sterile single-dose infusion products should be used and sterile infusion techniques (alcohol swab) should be used. The milking parlor should be kept clean. The teat dipper should be kept clean; organisms an survive in many germicides.

Must do’s

• Proper and regular disposal of excreta
• Disinfection of housing premises
• Sanitization of cow’s udders and milker’s hands or the milking machines prior to use.
• Prior and post milking teat dips with isopropyl alcohol, chlorhexidine and 1% sodium hypochlorite solution is effective.
• Thumb rule is to milk primiparous cows’ first and multiparous cows latter.
•  Among these healthy cows are to be milked first and mastitic cows milked at last.
• Hind quarter milking should preferably follow fore quarter milking.

 

 

General strategies to be adopted

Dry cow management

Dry cow management is important not only in preparing cows for the next lactation but is a key to prevent many disorders e.g., milk fever, abomasal displacements, retained placenta, uterine infections and clinical mastitis. Cows are most susceptible to new mastitis infections during the first two weeks of the dry period, the two weeks before calving, and the two weeks after calving. Dry cow therapy is 90-93% effective against subclinical Streptococcus agalactiae infections, 70-80% effective against Staphylococcus aureus, and 70-90% effective against environmental streptococci.

The 4 goals of Dry Cow Therapy

1. Cure existing infections at dry off.

• Reducing the number of cows carrying infections through the dry period not only prevents these flaring up into clinical infections but limits the source of contagious bacteria to other cows in the herd.

2. Prevent new infections at dry off and throughout the dry period.

• Dry period mastitis is difficult to treat, is costly and time consuming and can have long term effects on the cows’ production.
• Prevention is vital, especially where it is difficult to inspect the cows regularly during the dry period.

3. Protect against mastitis and reduce new infections around the calving period.

• Mastitis around calving is common. The cow’s defences are down around the calving period and there is plenty of exposure to environmental bacteria.

4. Reduce Somatic Cell Count (SCC) and mastitis into the subsequent lactation.

• Effective DCT will significantly reduce Somatic cell count

Dry cow therapy can be blanket i.e. for all cows drying off or selective i.e. only to cows tested positive for mastitis.  While dry treatment is very effective, it must be administered properly, and dry cows must have favorable environmental conditions. If the teat ends are not cleaned properly, there is possibility of injecting very high numbers of bacteria into the udder, which would overwhelm the antibiotic just administered. Unsanitary treatment procedures cause rather than eliminate mastitis.

There is no substitute to proper management of dry cows in mastitis control. If dry cows are exposed to muddy or dirty conditions, the risk of mastitis will increase. This is especially true at calving time; cows are under much stress during this period. If an udder is exposed to wet, dirty conditions, mastitis will increase.

Teat Sealant

The use of an internal teat sealant is an important part of a dry cow therapy program. The combination of Antibiotic Dry Cow therapy and Teat Sealant provides benefits over Antibiotic Dry Cow therapy use alone through improved prevention of subclinical mastitis and reduced ISCC in the first 60 d of lactation. Teat sealants are inert compounds that physically prevent mastitogens from entering the mammary gland through the teat end, an intervention that mimics the natural defence mechanism of a keratin plug, closing each teat canal at drying-off (Godden et al. 2003).

Teat Dips

Pre and post-milking teat antisepsis is regarded as the single most effective practice for the prevention of mastitis to reduce the new intramammary infection rate in dairy cows and to maintain a low level of mastitis. Chlorhexidine (0.2%), a commercial iodophor (1% available iodine), a hypochlorite (4% available chlorine and Tap water can be used.

Role of nutrition

Nutritional factors play a key role in enhancing resistance against mammary infections (Politis, 2012), and dietary/ancillary supplementation of micro elements such as, Zinc, Copper, Cobalt, Iron, Manganese, Chromium and Selenium is essentially required for  optimization of udder immunity (Scaletti et al., 2003; Politis, 2012). Micronutrients such as Beta-carotene, Vitamin A, C and E, lactoferrins, L-histidine provide enhanced immunity and antioxidative effect, which prevent alveolar tissue degeneration. Protein, vitamin A and zinc influence epithelial health and can impact physical defense barriers of the udder. Protein status will also influence the integrity of the smooth muscle teat sphincter. Quality and quantity of the keratin plug may be influenced by protein, zinc and vitamin A. A meta-analysis revealed that vitamin E supplementation, on average, reduced the risk of intramammary infection 14% and reduced SCC by 70% . Recommended feeding level (as per Nutrient Requirements of Dairy Cattle, 7th rev. ed., National Academy Press: Washington, DC).

• Vitamin E:1000 IU per day to dry cows
• Selenium : 3 mg/d for dry cows
• Copper :10 and 15 ppm of the diet
• Vitamin A: 110 IU/kg BW
• Vitamin D : 30 IU/kg BW for dry cows
• Zinc: 300 mg/day

Phytotherapy

Potential of plants with antibacterial, anti inflammatory, antioxidant and galactagogue effect can be explored. Regassa and Araya (Taddese et al., 2009) screened some herbal preparation against mastitis causing pathogens and got promising results.

• Common plants are;
  • Fenugreek (Trigonella graecum foecum),
  • Fennel (Foeniculum vulgare),
  • Asparagus (Asparagus racemosus),
  • Ashwagandha (Withania sonifera)
  • Giloy (Tinospora cordifolia)
  • Amla (Embilica officinalis)
  • Jivanthi (Leptadenia reticulata)

Essential oils

Essential oils are volatile secondary metabolites of low molecular weight derived from plants. These have antibacterial properties, with no reports of resistance after prolonged exposure to gram-positive and gram-negative bacteria, and no side effects on human health which makes them a potential weapon against bacterial diseases. Due to the antibacterial and antifungal characteristics of essential oils and their main components, they are increasingly studied for the control of microorganisms.

Cytokine therapy

Cytokines are low molecular weight regulatory proteins secreted by WBC. Owing to their Immunostimulatory properties , they enhance the immune status of mammary gland. Cytokine regulate the host defence by

1. Activating B cells, T cells, macrophages,
2. Induces clonal expansion of activated B, T cells and macrophages
3. Initiate secondary secretion of variety of other cytokines by activated lymphocytes.

Commonly studied cytokines in mastitis are Granulocyte Monocyte-Colony stimulating factor or Interlukin (IL-2), tumor necrosis factor and Interferons IFN (Sordillo et al. 1997).

 

 

Vaccination

Vaccination against mastitis has been tried (Sordillo et al. 1997) but due to the multiple etiological agents involved it is seldom used. Vaccinea are available against Streptococcus uberis , S. agaglactiae , Staph. aureus and E. coli. Vaccines against S. aureus and S. agalactiae contains either the whole organism (cellular lysates, inactive, and attenuated vaccines) or subunits (toxins, surface proteins, and polysaccharides). the mutant core antigen J5 is most commonly used against mastitis due to E. coli.

Prompt treatment

Sub-clinically mastitic cows should be identified and subjected to short term treatment with effective antibiotics at least for 3-5 days. The clinically affected animals should be provided immediate treatment and chronic cases should be segregated or culled. This is the only technique to remove the source of infection. An “extended therapy protocol” or “extended duration of therapy”, defined as administering intramammary treatment (mastitis tubes used in the quarter) for 2 to 8 days consecutively increases the chance of complete bacteriological cure of mastitis in which all of the bacteria in the gland causing the infection are killed. Antibiotics have been of value in controlling many infections, but they depend on judicious use to minimize the incidence of resistance forms (Danso and  Vlas , 2002). Complete cure often prevents relapses, prevents further damage to the mammary tissue, lowers somatic cell count, and helps to sustain future milk production.

Conclusion

Mastitis is a multifactorial disease that ensues due to management, host and environmental factors. Incidence of new cases can be reduced by adopting certain management changes as well as by boosting the host defense mechanism as well as udder immunity. Managemental alterations involve adopting dry cow therapy, supplementing antioxidants, providing prompt treatment to affected animals, phytotherapy, cytokine therapy etc.

 

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