MASTITIS: CHALLENGES AND SOLUTIONS

Introduction

One of the reasons for low productivity is poor animal health, particularly, mastitis which is single largest problem in dairy animal in terms of economic losses in India as well as all over world.

Bovine Mastitis

 mastitis is an inflammation of the mammary gland in response to injury for the purpose of "destroying or neutralizing the infectious agents and to prepare the way for healing and return to normal function.

Inflammation

can be caused by many types of injury including infectious agents and their toxins, physical trauma or chemical irritants. In the dairy cow, 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." 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. During milking, 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. 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 that are associated with high impact force against the teat end propel bacteria through healthy teat ends. This includes liner slips caused by excessive temporary vacuum losses, low vacuum reserve or level, and abrupt milking unit removal without shutting off vacuum, as well as vacuum fluctuations caused by inefficient vacuum regulation, blocked air vents, restrictions in the short milk tube, poor cluster alignment, or poor liner condition. After milking, the sphincter muscle in the teat canal remains dilated for 1-2 hours and bacteria present during this time can enter the teat canal. Examples would be dirty housing or environment, or failure to use teat dipping properly. An inflammatory response is initiated when bacteria enter the mammary gland and this is the body's second line of defense. These bacteria multiply and produce toxins, enzymes, and cell-wall components which stimulate the production of numerous mediators of inflammation by inflammatory cells. The magnitude of the inflammatory response may be influenced by the causative pathogen, stage of lactation, age, immune status of the cow, genetics , and nutritional status. Polymorphonuclear neutrophil (PMN) leukocytes and phagocytes 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. Somatic cells consist mainly of PMN or white blood cells. At the infection site, PMN surround the bacteria and release enzymes which can destroy the organisms. The leukocytes in milk may also release specific substances that attract more leukocytes to the area to fight the infection. 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.

Mastitis Causing Bacteria

Disease causing bacteria are often referred to as pathogens. The most common mastitis pathogens are

found either in the udder (contagious pathogens) or the cow's surroundings (environmental pathogens), such as bedding, manure, soil, etc. Contagious mastitis pathogens (Staphylococcus aureus, Streptococcus agalactiae) are spread from infected udders to "clean" udders during the milking process through contaminated teatcup liners, milkers' hands, paper or cloth towels used to wash or dry more than one cow, and possibly by flies. Although new infections by environmental pathogens

(other streptococci such as Str. uberis and Str. Dysgalactiae and coliforms such as Escherichia coli and Klebsiella) can occur during milking, primary exposure appears to be between milkings. Coliform infections are usually associated with an unsanitary environment (manure and/or dirty, wet conditions), while Klebsiella are found in sawdust. About 50% of environmental streptococci infections display clinical symptoms. Sixty to 70% of environmental pathogen infections exist for less than 30 days and are not easily detected. Subclinical infections are those in which no visible changes occur in the appearance of the milk or the udder, but milk production decreases, bacteria are present in the secretion, and composition is altered. There exits a negative relationship between SCC and milk yield. Many of the cows with SCC over 200,000 may have subclinical mastitis.

Effect on Milk Composition

Mastitis resulting from major pathogens causes considerable compositional changes in milk, including

increases in SCC. The types of proteins present change dramatically. Casein, the major milk protein of high nutritional quality, declines and lower quality whey proteins increase which adversely impacts dairy product quality, such as cheese yield, flavour and quality. Serum albumin, immunoglobulins, transferrin, and other serum proteins pass into milk because vascular permeability changes. Lactoferrin, the major antibacterial iron-binding protein in mammary secretions, increases in concentration, likely because of increased output by the mammary tissue and a minor contribution from PMN. Milk protein breakdown can occur in milk from cows with clinical or subclinical mastitis due to presence of proteolytic enzymes. Plasmin increases proteolytic activity by more than 2-fold during mastitis. Plasmin and enzymes derived from somatic cells can cause extensive damage to casein in the udder before milk removal. Deterioration of milk protein as a result of mastitis may continue during processing and storage. Mastitis increases the conductivity of milk and sodium and chloride concentrations are elevated. Potassium, normally the predominant mineral in milk, declines. Because most calcium in milk is associated with casein, the disruption of casein synthesis contributes to lowered calcium in milk.

Effect on dairy industry

Mastitis is responsible for heavy economic losses due to reduced milk yield ( up to 70%), milk discard after treatment (9%), treatment costs (75), premature culling (14%), decrease in milk quality and price due to high bacterial / somatic cell count, increased risk of subsequent mastitis, herd replacement, antibiotics residue in milk and its products and rejection by processor and consumer. Though cows with clinical mastitis have more dramatic changes in milk yield and composition than cows with subclinical mastitis, the losses due to latter are more severe than those due to the former. The Indian diary industry suffers and annual loss of approximately 526 millions dollars due to mastitis, 70% of which is due to subclinical  mastitis.

           

Diagnosis

While acute clinical mastitis is easily suspected/recognized While acute clinical mastitis is easily suspected/recognized even by farmers and is readily diagnosed due to udder swelling, pain and drastic decrease in milk production, the sub-clinical mastitis has neither visual abnormalities in the mammary gland (swelling, hotness, cracks etc.) nor in the milk (blood, clots, flakes etc.). Therefore, routine physical examination of udder and diagnostic screening tests for early detection of mastitis and proper treatment of affected animal are of paramount importance in order to minimize losses due to sub-clinical and clinical mastitis.

Treatment and control: The treatment of the Mastitis is definitely more expensive than its control. Needless to mention in Clinical Mastitis parenteral and intra-mammary antibiotics are used. The word of caution is the judicious use. The intra-mammary use of antibiotics should be avoided to the best possible extent as this is likely to create more damage to udder.

Some of the control measures are as mentioned below:

1. The best possible way is to regularly examine the udder milk for possibility of Sub-Clinical Mastitis.

2. The udder and the teats should be washed pre and post milking with clean water.

3. Herbal teat-dip should be used for cleaning and disinfecting the udder.

4. Post diagnosis of Sub-Clinical Mastitis. Mastilep should  be applied with gentle hand on udder during post milking.

5. The Veterinarian should be consulted for farm management, prevention/control and treatment of mastitis.

Conclusion

Mastitis not only reduces the productive capacity of the cows, it is also expensive to treat. Therefore, its prevention should be the prime concern of each farmer. Effective mastitis control strategies including prudent use of antibiotics, adequate strategies including prudent use of antibiotics, adequate housing with proper sanitation and regular screening for early detection and treatment, follow up of chronic case, culling of older cows with repeated attacks, avoiding consecutive milking and susceptibility testing of the mastitis pathogens before treatment are recommended to alleviate the problem.