In the present state of knowledge it seems practicable and reasonable to define mastitis as a disease characte- rized by the presence of a significantly increased leukocyte count in milk from affected glands.
The Mastitis Committee of the Australian Veterinary Association defined nature and causes of mastitis as “Mastitis is an inflammation of udder and as such is a disease complex resulting from any condition or combination of factors leading to injury to the internal structure of one or more quarters”.
There is no standard definition of various types of mastitis but is simplest to consider mastitis as clinical or sub-clinical&symptoms may be acute or chronic.
This is characterized by heat, pain and swelling or in duration, which may occur with or without these signs. The udder secretion is usually abnormal; milk yield and quality are usually markedly affected. Several factors influence the severity of the effects e.g., organism responsible, the susceptibility of the cow and the extent of udder damage.
A quarter infected with a pathogen, having an increase in the cell content of the milk and the absence of clinical signs, is generally accepted as being affected with sub-clinical mastitis. Indirect tests such as California Mastitis Test (Rapid Mastitis Test in Australia), cell count or white side test are required to make the diagnosis. The level of cell count regarded as significant varies with different workers, but counts in excess of 500,000 cells per ml are generally regarded as indicative of sub clinical mastitis. This form of mastitis is frequently not noticed by the farmer.
This refers to infection with mastitis organisms, which has not produced changes coming within the deficiency of sub clinical mastitis. This condition is most common with staphylococci and streptococci. Most potentially pathogenic bacteria have been implicated at one time or another in causing mastitis, as have yeasts and Mycoplasma organisms. However, Str. agalactiae, staph aureus, other streptococci and Gram-negative bacilli (including E. coli and Pseudomonas spp. etc.) account for probably 99% of all mastitis. It is clear that the first two infections are the more important and probably staphylococci are now the commonest organisms associated with mastitis.
Mastitis is a disease of all milking animals. It is common in dairy cattle, uncommon in beef cattle. In cattle it is characterized by changes in the udder tissue, clots and changes in the constitution of milk, and is sometimes accompanied by heat and pain in the udder.
When we think of the extreme complexity and delicacy of the mammary gland, the fact that it is pummeled along between the hind legs of the cow, lain on, kicked, horned; that it contains milk, a suitable medium for the growth of a great number of bacteria, fungi and other micro-organisms; that such milk is open, via the teat canal to contamination and is interfered with at least twice a day, it is surprising that any cow ever escapes mastitis.
Added to this, by selective breeding the gland has been developed to an abnormal size and selected to secrete a grossly abnormal amount of a natural product.
It is thus apparent that particular efforts must be made to treat the udder with every possible care to eliminate predisposing causes which include, the presence of chronically affected carriers in the herd, the use of dirty methods of milking which transfers infectious milk from animal to animal, and faulty milking machines which may by excessive suction, cause damage. Faulty sphincter of the teat may give imperfect closure of the teat canal and facilitate infection. Sores at the opening of the teat canal probably play an important part in allowing the germ to enter. Infection with contagious abortion, and also an inherited predisposition are predisposing causes mentioned by some authorities. Feeding a high protein grain ration apparently renders the udder more liable to infection. Chronically, infected udders are liable to “Flare up” into the acute form. Faulty milking, filthy conditions and the presence of flies may all play a part in assisting the spread of the disease. Mechanical injury of the udder will, of course, act as a definite predisposing cause.
It is important to realize that milk is secreted, in part, by erectile tissue in the udder becoming turgid with blood. Unless the cow is settled and contended and enjoys milking time, it does not occur. Such reaction is a conditioned reflex. Thus, if a cow is accustomed to being washed with water, say one minute before she is milked, her ductless glands will so secrete their hormones that at this given time after the washing with warm water the erectile tissue will become turgid and the milk will flow into the teats. As the farmers say “she lets down her milk”. This “letting down” the milk is conditioned in response to all the usual happenings. These happenings should be so masterminded that each event becomes a pleasuring device. The wise farmer “woos” fickle female bovines to yield up all their milk by “pleasuring” the erectile udder tissue to climax and so “let down” the milk.
Thus, if the cow has her udder washed at a longer period than usual before milking is commenced or if she comes into the bail (stanchion or tying place) out of order, or is forced to go into the wrong bail or is otherwise upset (e.g. by the presence of dogs or strangers, kicks or horning), the secretion of milk may be interfered with. Under such circumstances the udder is not milked out and this may have a major effect in precipitating outbreaks of mastitis. In practice the employment of a new milking hand or some sharp change in procedure is often noticed to coincide with the occurrence of mastitis.
Music in bails has been found to have a considerable effect on the contentment and milk secretion of the cows. Cows particularly some nervous and highly-strung breeds, accustom themselves to particular persons. It is well known that some attendants with a good “animal sense” have a vast influence on the contentment and production of the animals they handle. In control of mastitis this factor of the wise contended handling of cows is of the very greatest importance.
The features of chronic bovine mastitis were closely resembled with the features of tissue allograft undergoing rejection. Workers further showed that milk is rich in leukocytes and, if milk from one cow is injected into the quarter of another cow previously milked out, the foreign leukocytes stimulate an allogenic lymphocyte transfer reaction. They further pointed out that a pipeline milking machine might transfer milk from one cow’s udder into the empty udder of another cow when it is incorrectly managed. They consider that in some cases this may be an important predisposing cause to clinical mastitis in a cowshed.
The incidence of heifers shedding “staphylococci” in the milk increased from very low levels to approximately 50% by 8 weeks. When heifers were milked separately from older cows, through teat cups that were chemically sterilized between milking, under these conditions the number of heifers shedding “staphylococci” during their first lactation was on average 10% or less.
In a complex disease such as mastitis, predisposing factors are manifold. Smith et al. (1984) showed that selenium deficiency is associated with increased susceptibility to mastitis. Other workers showed that it is also associated in cattle with retained fetal membranes, ill thrift, reproductive disorders and reduced response to some bacterial infections. Thus, in selenium deficient areas the provision of proper dose of selenium will helpful in preventing the mastitis. Ryan et al. (1987) produced good controlled evidence that selenium deficiency predisposes to staphylococcal mastitis infection. It has been shown that pastures high in estrogens may predispose cows to mastitis.
a. Susceptible Animals
All breeds of dairy cows are susceptible. It is generally held that high producers are more commonly affected than poor producers. With succeeding lactations, the liability to have contracted infection increases. That is, more cows on fourth calf than cows on their first calf are affected.
b. Mode of Infection
All modes of infection may operate. The causal bacteria may be transferred by the hands of the milkier, by milking machine cups and by flies, or the cow may be infected directly by lying on contaminated ground. Infection may be up the teat canal, through the blood stream or through skin injuries. Apparently, the mode of infection tends to vary with each bacterial type. In some cases it has been shown that the organisms grow up the teat canal, cause inflammation of the milk cistern at the base of the teat and then spread to other parts of the gland, causing inflammation of the whole quarter. In case of “streptococcus agalactiae”, the main mode of infection is via teat canal, and this fact lies behind nearly all the hygienic methods of control recommended.
Cows that have been affected or are recovering from one attack do not remain immune to further attacks.
Signs And Symptoms:
A wide range of differing symptoms will be shown with different types of infection. Milk may become watery or thickened or pus-like, and may contain clots which vary in color from yellow to blood clots. The clots may also vary considerably in character. In some infections they are large, slimy clots. Other clots may be purulent; some infections produce mealy or flaky clots. Some clots may consist of fine flocculation that is seen like small pieces of blotting paper. The nature of the milk may be changed in all sorts of ways. Thus, on some occasions, it is merely thinner and paler. It may be thickened and amber in color, darkened, or blood stained, and have varying degrees of unpleasant smell. Milk production may be decreased or ceased altogether and be replaced by pus, clots or watery material. The condition of the udder may become hot, tense, and painful and later develop fibrotic changes with hard lumps, or it may be shriveled and wasted. In some severe types, one or more quarters of udder may die and slough right off leaving a filthy, gaping wound. In severe cases the animals will show general symptoms of toxemia or septicemia, being off their feed, shivering and scouring and may die.
Management And Mastitis Spread:
Decreasing Exposure to Pathogen between Milking
The microorganisms are abundant in the surroundings in which cows live, including manure, soil, bedding, feedstuffs, water and plant material. Where poor hygiene exists, housed cows are at greater risk of infection with environmental microorganisms than cows on grassy pasture. However, where good hygiene practices exist, housed cows may be at less risk than cows on pasture that have access to ponds, mud holes, or wet lots. The prevalence of clinical cases increases with confinement; especially during winter months.
Environmental conditions that can increase exposure to these microorganisms include overcrowding, poor ventilation, inadequate manure removal, poorly maintained free stalls, access to farm ponds, dirty calving areas, and general lack of farm cleanliness and sanitation. Maximum air movement through housing, feeding and calving facilities should be provided to reduce the number of these microorganisms; especially airflow over bedding materials, floors, and walkways. Moisture of any kind such as rain, humidity, urine, drinking water and even udder wash favor the growth of environmental microorganisms.
Recommended Bedding Materials:
Low-moisture inorganic materials such as limestone, sand and clay are preferable to finely chopped organic materials because they contain few nutrients for bacteria to utilize and harbor and are therefore associated with lower numbers of microorganisms. Of these, washed sand is often recommended because of greater ease in handling and because it is less likely to harden in stalls if the material becomes wet.
The key to successful use of any of the materials is daily replacement of wet and soiled bedding and regardless of the material used, this practice has been shown to reduce bacteria counts. Composting solid wastes for bedding material has been attempted, but it contains excessive numbers of coliform bacteria once it is placed into free stalls. Alternative bedding that has been evaluated is recycling newspaper, but little advantage was gained in decreasing bacterial counts which are similar to those in chopped straw. However, it may be an economical alternative.
Prevention of Mastitis by Good Milking Procedures
1. Provide cows with a clean, stress-free environment
• Milking time should be a consistent routine.
• The cow should not be frightened or excited before milking because such stress results in secretion of epinephrine in blood stream which interferes with normal milk let down.
• Udders should be clipped or singed as necessary to remove long hair and reduce amount of dirt, manure and bedding that may contaminate milk.
• Hands of person milking the cows be washed and dried before milking. Gloves are also beneficial. Hands/gloves be rinsed in disinfectant solution before and after milking each cow in a herd.
2. Check the foremilk and udder for mastitis
• Strip cups and plates should be cleaned and sanitized after each milking to prevent the spread of mastitis organisms.
• Stripping of milk directly onto the floor, followed by immediate hosing of the floor surface can be done and incorporation of black tiles into the floor of parlor facilitates this procedure.
• Milk should never be stripped directly into the milker’s hand because this procedure spreads microorganisms from teat to teat and cow to cow via contaminated hands.
3. Wash teats and the Ventral surface of the udder with a warm sanitizing solution
• Correct washing and massaging of teats and udder sends a signal to pituitary gland that secretes oxytocin that causes milk let down.
• In stanchion barns a sanitizing solution should be used in bucket with individual cloth or paper towel to wash the teats.
• Use of a common cloth or sponge should not be permitted because these become grossly contaminated and may cause mastitis spread.
In large dairy herds, milking facilities may be equipped with sprinkler pens where 80 to 120 cows are group washed. After providing them sufficient drip-drying time before cows enter the milking parlor their teats and udders be completely dried.
4. Use a pre-milking Teat Dip
Pre-milking teat dip reduces infections with environmental microorganism by about 50%. Recommended pre-dipping procedures are as follows: clean teats, forestrip predip teats and allow recommended contact time (usually 20-30 seconds), dry teats with an individual paper towel to remove germicide residues and attach milking units.
Pre-dipping is sometimes done without prior washing of the dirty teats, and germicide is often placed on top of manure and dirt present on teat skin. This practice is not likely to reduce incidence of mastitis and somatic cell count, and will probably reduce milk quality. Manure and dirt must be removed to get full benefits of predipping.
5. Dry teats thoroughly
The milking of wet teats also promotes squawking of the teat cup liners, which may result in teat end impact.
6. Attach teat-cups within 1 minute
Attachment of teat cups should be done carefully to prevent the entrance of excessive air into the milking system. Maximum internal udder pressure is reached approx. 1 minute after udder preparation is begun and lasts for about 5 min. Since the majority of cows will milk out in 4 to 6 min, the consistent attachment of teat cups 1 minute after the beginning of stimulation makes maximum use of milk let-down hormone oxytocin.
7. Adjust milking units as necessary
• Teat cups that are seated excessively high on teats cause irritation to the lining of the teat and may contribute to the development of mastitis. Improperly aligned milking units may also block milk flow, increase strippings and slip more often.
• It is important that slipping or squawking of teat cups be minimized because such occurrences probably contribute to more machine-induced infections than any other single factor.
• If liner slips occur at the same time as the liner opens, tiny droplets of milk may be propelled against the end of the teat at very high velocity. Such droplets may contain mastitis-causing microorganisms and may penetrate the teat canal. Since milk flow slows near the end of milking the chances of the microorganisms being flushed out of the teat are reduced and an infection of the quarter may result.
8. Shut off vacuum before removing teat cups
The goal should be to remove teat cups just as the last quarter milks out, but vacuum should always be shut off before teat cups are removed. An increased risk of infection exists when teat cups are removed while under vacuum.
Dip teats with a safe and effective teat dip:
Teat dips in addition to killing all microorganisms on teats reduce teat canal colonization and help to heal teat cup lesions. The list of teat-dip germicides includes iodophores, chlorohexidines, linear dodecyle benzene sulfonic acid (LDBSA), sodium hypochlorite, sodium chlorite/lactic or mandelic acid, hypochlorous acid, quaternary ammonium and antimicrobial proteins and fatty acids.
Only products shown by research to be safe and effective should be used. This involves using a product registered with the FDA or concerned regulatory authorities.
Problems related to teat dips:
Some teat dip germicides may cause harmful effects on teat skin and cause chapping. The irritation might be due to low or high pH or high titratable acidity or alkalinity or a formulation. Because of the potential for irradiation, skin-conditioning agents often are added to teat-dope formulations. Glycerin is an example of humectants, a substance that promotes the retention of moisture. Emollients, substances that soften and smooth the skin also are found in dips; linolin is a popular choice and coats the skin and reduces evaporative water loss. The only difficulty is that germicidal activity of teat dips may be reduced if concentrations of humectants and emollients become too high above 10 or 12% of the total dip.
Normal teat skin is coated with bacteria static acids that retard the bacterial growth. When exposed to cold, wet and windy conditions, teat skin may become chapped and irritated. Also protective surface coating may be removed, allowing bacterial growth on teat skin.
Basically, if equipment is operating according to the recommendations, and its capacity is not exceeded, the machine itself contributes little to the mastitis problem. However, the milking system can influence the development of mastitis causing bacteria from one cow to the next. Improper use, such as failing to shut off vacuum when teat cups are removed, may injure the teat canal and increase susceptibility to infection. Irregular fluctuations in milking vacuum may cause tiny droplets of bacteria-laden milk to impact against the end of the teat, propelling mastitis-causing bacteria through the teat opening and into the udder. Therefore, it is important to dry teats before milking, position the milking unit properly on udder, select appropriate liners, avoid excessive machine stripping, and minimize sudden air losses when machines are removed. Some experts claim that changing liners every 1000 to 1200 milking or every 60 days, whichever comes first will reduce risk of new infection.
The losses caused to the dairy industry by this disease are enormous. Almost every herd suffers intermittent losses from good cows going ‘light’ or going blind in various quarters. The aggregate loss to the industry is one of the major deductions from economic production. It is probable that in some herds more than 15% of cows are rejected each year because of mastitis. Some cases of mastitis are caused by “streptococci” of human origin the type that produce septic sore throat and scarlet fever. These are a danger to the consumers of milk but are fortunately rare.
The National Mastitis council (USA) shows that, when bulk tank SCC is 200,000, about 6% of quarters in the herd could be expected to be infected. At 500,000 SCC 16% of quarters are likely infected with a 6% reduction in milk production.
Thus, mastitis causes heavy losses in terms of costs of rearing cattle and heavy losses follow from early disposal before they have reached their maximal reduction.
Dr Syed Hassan Raza
Department of livestock mangement
Faculty of animal husbandry