Mastitis is a complex disease, because it has numerous causative bacteria, and no single control measure will prevent infections by all pathogens. However, the basic concepts for the control of the contagious pathogens Staphylococcus aureus and Streptococcus agalactiae have been known for over 30 years. Despite this fact, mastitis continues to cause losses in the dairy industry of nearly $2 billion in the United States each year (1, 3). This translates to an annual loss of approximately US$18,000 in a 100 cow herd. The majority of this loss is in reduced milk production due to the presence of infections. Effective programs of post-milking use of germicidal teat dips, strict milking time hygiene, dry cow therapy, and culling can result in the eradication of Strep. agalactiae from dairy herds and a markedly reduced incidence of Staph. aureus. These management approaches, directed at preventing infections, must be used properly and consistently to provide continued success toward controlling contagious mastitis.

Infections of the mammary gland by pathogenic bacteria result in decreases in milk production and compositional changes that vary with the intensity and duration of the infection (3, 8). Compositional changes include decreases in lactose, fat, casein, and calcium and increases in sodium, chloride, and blood proteins in milk (14). Subclinical infections are those with no visible changes in the appearance of the milk or the udder, but milk production decreases, bacteria are present in the milk, and composition is altered. Clinical mastitis is characterized by abnormal milk and swelling or pain of the udder; it may be accompanied by systemic signs such as elevated rectal temperature, depression, or decreased feed intake. As in subclinical mastitis, milk production declines, bacteria are present in the milk, and dramatic changes in milk composition are usually present. Chronic mastitis is an infection that is long duration and may show periodic clinical symptoms.

One of the early events of an infection is the movement of white blood cells or leukocytes into the udder to fight the infection (8). The end result is an increase in the number of cells or somatic cell count (SCC) in milk . All milk contains cells, but the number of cells depends on the presence or absence of infection. The normal SCC of milk from uninfected cows is less than 200,000 per ml. Milk from first lactation cows may be below 100,000 per ml. Thus the SCC of milk from individual quarters, individual cows, or from the bulk tank is commonly used as an indicator of udder health. Table 1 shows the relationship of SCC in the bulk tank with infection level in the herd and estimated loss of milk production due to mastitis (4). It is obvious from this table that elevated SCC mean more mastitis and less milk production. The goal should be to lower the SCC in bulk tank milk as much as possible. This is accomplished by reducing the number of new infections through mastitis control measures discussed below and by removing chronic mastitis cows from the herd; chronic cows often contribute a high proportion of the SCC in the bulk tank. A simple cowside screening test to indicate relative somatic cell level for individual cows is the California Mastitis Test (CMT), sometimes called a paddle test (3).

Staphylococcus aureus and Strep. agalactiae are the common contagious mastitis pathogens (3, 28). The major reservoir for these pathogens is the infected udder, and infections are spread among cows or between quarters during the milking process by contaminated milking equipment, milker's hands, or cloths or sponges used to wash or dry more than one cow. Infections tend to be chronic (i.e., long duration) and subclinical with periodic clinical episodes. Thus contagious mastitis results in decreases in milk production and increases in bulk tank SCC, but there may be few visible symptoms, i.e. this tends to be a hidden form of mastitis. Herds with high bulk tank SCC tend to have high levels of infections by contagious pathogens.

Streptococcus dysgalactiae is generally characterized as an environmental pathogen, but also may have characteristics of a contagious organism and appears to spread from cow to cow (28). This pathogen is generally responsive to teat dipping and dry cow therapy, but new infections can occur in a herd when no other udder infections by this organism are present. Corynebacterium bovis is considered a minor pathogen (9). The main reservoir appears to be infected udders or teat ducts, and this organism is spread rapidly from cow to cow in the absence of adequate teat dipping. Infections by C. bovis cause only moderate inflammation with SCC exceeding those of uninfected glands by only two- to threefold. Infections are infrequently the major cause of elevated bulk tank SCC, clinical mastitis, marked compositional changes, or dramatic decreases in milk production.

Mycoplasma species are contagious pathogens that are rare in some areas but not uncommon in others (5). Mycoplasma bovis is the most common species and probably causes the most severe problems. Some characteristics of mycoplasma mastitis include sudden onset, rapid spread in the herd, marked reduction in milk production, and resistance to treatment. Veterinary assistance is recommended for the diagnosis and control of mycoplasma mastitis, because special bacteriological culture procedures are necessary for diagnosis.

Prevention is the key to controlling mastitis, not treatment. Treatment is an attempt to eliminate an infection that has already occurred and should be limited to clinical cases. Mastitis control based solely on antibiotic therapy during lactation is both costly and ineffective. Prevention is based on reducing the number of bacteria to which the teat end is exposed; for contagious pathogens this involves reducing cow to cow spread. Effective control measures differ for contagious and environmental pathogens (3, 10). The basic management procedures which have been shown to have the greatest effectiveness in preventing contagious mastitis are discussed below.

Teat Dipping and Dry Cow Therapy. Teat dipping and dry cow therapy form the basis of mastitis prevention programs (1, 28). An effective germicidal teat dip should be applied to all teats at the end of milking to kill contagious bacteria that were deposited on the skin during milking. This is the single most effective method of preventing new infections by contagious pathogens. Teat dipping alone can reduce new infections by contagious bacteria by 50%. Examples of some teat dips that have historically been effective are those that contain 0.5 to 1.0% iodine (iodophor), 4.0% hypochlorite, or 0.5% chlorhexidine acetate. Numerous other efficacious products are on the market today, but only products that have been tested and shown to be effective in reducing new infections should be used. An 18 month study (22) using a teat dip containing chlorous acid and chlorine dioxide showed 63.8% reduction of new Strep. dysgalactiae infections. Of the environmental streptococci, Strep. dysgalactiae seems to be controlled more readily by milking time hygiene. The question frequently arises, "How much of the teat should be covered with dip?" There is no magical answer to this, but the safest approach is to cover all of the teat that was touched by the inflation or liner. Spray application of germicide can be as effective as dipping, if all the teats and teat ends are covered. However, the human tendency is to spray too rapidly and get poor coverage. Therefore, dipping often proves to be the best method of application.

The intramammary treatment of all quarters of all cows is recommended after the last milking of the lactation (at drying off) with a commercial antibiotic tube designed for use in the dry cow (3). Dry cow therapy is more effective than lactation therapy in eliminating existing infections. Also dry cow therapy will reduce the number of new infections in the dry period, and a higher concentration of antibiotic can be used without risk of antibiotic residues in milk. Always apply teat dip after the intramammary infusion of an antibiotic.

The consistent use of a regimen of teat dipping and dry cow therapy has been shown to be effective in reducing the level of infection in commercial herds with predominantly Staph. aureus and Strep. agalactiae mastitis (13, 18). Figure 1 shows that it takes one to three years for significant improvement with these procedures alone. To stop using these methods of control results in a rapid return to the infection level present before initiating control measures. These findings reinforce the need for continued use of mastitis control procedures on farms.

Milking Time Hygiene. Strict milking time hygiene is a high priority to reduce spread of contagious bacteria from one cow to another and to reduce bacterial contamination of the bulk tank milk (19). Many acceptable practices may be used to prepare the teats for milking. However, teats should be clean and dry before applying the milking unit. The use of a germicidal udder wash is recommended, but rinsing a contaminated cloth or sponge in a germicide solution will not kill all the bacteria in the cloth . Therefore, do not use the same cloth or sponge to wash or dry all cows, because this practice will spread bacteria from one cow to another. Use individual cloth or paper towels to clean or dry each cow. Keep milking equipment properly cleaned and in good operating condition. Anything that causes liner slippage may increase the chance of spread of infections from one infected quarter to other quarters of the same cow.

Automated backflush systems effectively sanitize milking units between cows and reduce spread of contagious pathogens (11). However, these systems are expensive and the cost may not adequately justify the added benefit over strict hygiene and teat dipping. English studies (19) evaluated the effects of "partial hygiene" (rubber gloves, disinfectant udder wash, individual cloths, teat dipping) and "full hygiene" (partial hygiene plus pasteurization of milking clusters for 5 seconds using water at 85°C) on new infection rates. The "full hygiene" reduced new infections by 58% compared with no hygiene, but even the "partial hygiene" reduced infections by 44%.

These studies and others (12) strongly suggest that the only effective methods of cluster disinfection are mechanical backflushing systems or pasteurization using hot water (85°C). Dipping a cluster in water or a germicidal solution after milking each cow is not effective. If proper teat dipping is used after each milking, even effective cluster pasteurization results in small additional benefits.

Predipping. Predipping, i.e. use of germicidal teat dip before milking to sanitize the teat, has been shown to reduce environmental mastitis by 50% (24). However, predipping has no reported benefit in controlling contagious pathogens, because contamination of teats will occur after its use. Teat dipping with germicidal or barrier teat dips during the dry period has no added benefit in preventing mastitis (17, 26).

Culling. Culling is a necessary part of control of mycoplasma mastitis and will play an important role in reducing the number of Staph. aureus infected cows in a herd (5, 28). Culling chronic mastitis cows which have not responded to treatment eliminates a source of contagious bacteria (the infected cow), reducing the risk of new infections in other cows. The level of infection in the herd and the bulk tank SCC are immediately affected. However, culling decisions should be made after effective milking time hygiene and teat dipping programs are in place in order to gain long term benefits.

Segregation. Herds with a significant Staph. aureus or mycoplasma problem may benefit from a program of segregating infected cows and milking them last (5). The success of segregation appears to be dependant upon the adequate identification of infected cows; this is usually done by culturing of milk samples and can be quite expensive. As mentioned above culturing milk samples for mycoplasma requires special culture techniques. Stamp (30) reported successful identification of Staph. aureus infected cows in a segregation program using monthly SCC results from the DHI program, CMT, and culture results. He concluded that Staph. aureus infected cows must be identified early and segregation required maintenance of records and management time.

Lactational Therapy of Clinical Mastitis. Antibiotic therapy during lactation has generally been successful in Strep. agalactiae problem herds (3, 5, 28). In contrast, the treatment of Staph. aureus infected cows during lactation is of limited value, because cure rates are usually less than 50%. Antibiotic therapy of clinical cases may reduce clinical symptoms but does little to improve the prevalence of infections in the herd; most of the udder infections are subclinical and go undetected. Mycoplasma infections are not responsive to antibiotic therapy.

Vaccines. Prevention of Staph. aureus mastitis also has been attempted through the years by the development of Staph. aureus vaccines (reviewed in 29; 2). Common results have been reduction in clinical episodes and an increase in spontaneous cure rate. Even the most successful attempts have not approached the success in controlling the disease that is achieved by teat dipping. However, if successful Staph. aureus vaccines are developed in the future, immunization will remain a tool in the control of mastitis and must be only a part of the total management scheme.

Today we recognize that heifers may also calve with Staph. aureus infections (7, 27). The prevalence of Staph. aureus in heifers appears to vary considerably among herds. Trinidad et al.(31) found 14.9% of 370 quarter secretion samples were positive for Staph. aureus in 37.1% of 116 breeding age and pregnant heifers in four herds. In Kentucky (15) we observed that 3.8% (106 heifers) and 3.3% (60 heifers) of teat canals from heifers 1 day to 24 months of age were positive for Staph. aureus. An extensive study of 18 dairy herds by Washington State University researchers (25) indicate that approximately 8% of heifers at calving had Staph. aureus udder infections. The prevalence of Staph. aureus in the lactating cows in these herds varied from less than 1% to 65% of cows at the beginning of the study. A survey of about 1600 breeding age heifers from four regions of the US showed 2.9% of quarters were positive for Staph. aureus (6). These results confirm that the prevalence of Staph. aureus is variable and that they may be harbored in the mammary gland as well as other body sites of virgin and pregnant heifers.

The prevalence of Staph. aureus has also been studied during the peripartum period in first lactation heifers. Schultze et al.(26) isolated Staph. aureus from 4.7% of quarters in first lactation heifers during the peripartum period. The high proportion of new intramammary infections (IMI) caused by Staph. aureus in first lactation heifers (13.1%) compared with cows (2.9%) was unexplained. Matthews et al. (16, 17), in a study evaluating the use of a barrier teat dip with germicide during the prepartum period, obtained teat orifice swabs 14 days prepartum and foremilk samples at parturition and at weeks 1 through 5 postpartum from first lactation heifers and cows. Quarter infection prevalence by Staph. aureus was 7.6% at calving, but declined by about 50% during the first week of lactation. The prevalence of Staph. aureus during the prepartum period in first lactation heifers was 3 times that observed in older cows. Oliver and coworkers (21, 23) found the prevalence of quarter infections by Staph. aureus in the peripartum period was 1% or less. Roberson et al. (25) showed that 43% of heifers having Staph. aureus IMI at calving remained infected at a subsequent sampling. They did not find a significant relationship between herd Staph. aureus prevalence and prevalence in heifers at calving.

Newbould (20) stated that eradication of Staph. aureus from individual herds may be possible, although more difficult than that of Strep. agalactiae. It was suggested that, with concerted hygienic efforts in lactating cows and removal of infected udders as a source, there would be a disappearance of Staph. aureus from other sites on the cows's body as well. The source of Staph. aureus in heifers is not understood nor are the methods of transfer. However, carriage sites on the lactating cow, including the vagina and nares, must be suspect. It is not known if elimination of Staph. aureus IMI from the lactating herd will result in disappearance from other sites such as from skin and mammary glands of heifers. The possibility exists that flies may serve as a vector. IMI of older cows remains the major reservoir of Staph. aureus in a dairy herd. However, it is important to recognize that heifers at calving can be another source of introduction of Staph. aureus into the herd.

A comprehensive contagious mastitis control program based on prevention will pay off with fewer losses associated with mastitis, improved quality of milk, and greater milk production. Such programs are based on sound management and include the following:

1. Strict milking time hygiene.

2. Post-milking teat dipping.

3. Dry cow treatment of all quarters of all cows.

4. Use properly functioning milking machines.

5. Cull chronic mastitis cows.

6. Use of segregation if practical.

7. Treat new clinical cases promptly

These procedures, including culling, can help to eliminate Strep. agalactiae infections from the herd, because the infected udder is the only source of this organism. Once all Strep. agalactiae infections are eliminated from a dairy herd, the herd will remain free of the organism unless infected cows are purchased. Although eradication of Staph. aureus is not likely, good control measures can reduce spread and keep infections to a minimum. A general goal is to reduce the SCC of the bulk tank milk as much as possible. Culling chronic cows will have a great impact initially on lowering the SCC in most herds, but sound control practices must be in place. A bulk tank SCC of 300,000 per ml or less is a reasonable goal to keep in mind.

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