Mastitis Control: The Basics

Lawrence K. Fox

College of Veterinary Medicine

Washington State University

Introduction

Mastitis is defined as inflammation of the mammary gland. That inflammation is characterized by the clinical and subclinical state. With the clinical state, the udder is warm to the touch, the skin appearing more red than normal, the cow may express pain when the udder, especially the teat of the affected mammary quarter, is touched, and the udder or the affected quarter will be swollen. Often the secretion from the infected mammary quarter will appear abnormal. The milk will be serous, with clots or flakes appearing in the milk. These clots and flakes comprise what is termed: “gargot”. Yet for every 1 case of subclinical mastitis, there are 50 cases of sub-clinical mastitis. Sub-clinical mastitis is characterized by reaction to tissue injury and loss of function. The reactions to tissue injury are manifested by slight changes in the milk composition: decreases in lactose, casein, and increases in ions and leukocytes. Loss of function is seen as lost milk production. These changes in milk yield and composition can not be seen with the naked eye, and therefore laboratory and cowside tests are used to detect the changes. Whereas the loss of function and reaction to tissue injury are also seen in clinical mastitis, in the subclinical state they can pass unnoticed.

Mastitis is almost always a result of a microbial infection, namely a bacterial infection. The mastitis pathogens can be classified as either contagious or non-contagious. The non-contagious can be classified as either environmental or opportunistic. The contagious mastitis pathogens of greatest concern are the Staphylococcus aureus, Streptococcus agalactiae, and Mycoplasma sp., with M. bovis and M. californicum the primary Mycoplasma sp. The environmental mastitis pathogens of greatest concern are the coliforms: Eschericia coli and Klebsiella sp.; and the environmental streptococci, Streptococcus uberis and dysgalactiae. The opportunistic pathogens are the coagulase negative staphylococci. Staphylococcus aureus and the coagulase negative staphylococci can be differentiated by their ability to coagulate blood plasma, with S. aureus being coagulase positive.

Prevalence of pathogens associated with mastitis

Pathogen type / %of quarters infected with mastitis pathogen (n=23735) / %of cows infected with mastitis pathogen (n=4957)
Environmental Streps / 3.9 / 11.5
Coliforms / 1.3 / 5.0

S. aureus

/ 4.0 / 11.5
S. agalacitiae / 4.3 / 6.5
Coagulase neg. staphs / 10.1 / 25.0

Mycoplasma sp

/ ? / ?

From the above table, it is clear that the coagulase neg staphs, the opportunists, are the most prevalent pathogen associated with mastitis. However, this pathogen type is rarely associated with clinical infections and only causes a mild inflammatory state. Moreover, infections by these mastitis pathogens are generally short lived. Mycoplasma mastitis infections were not part of this survey.

Reservoirs and Fomites of infection.

The reservoirs of the classes of mastitis pathogens are similar within class, and different between classes. The contagious pathogens have as their reservoir the mammary gland. Whereas S. agalactiae is an obligate udder parasite, S. aureus and the mycoplasma will infect and colonize other body sites, and perhaps environmental sites. Moreover, mastitis by S. aureus and the Mycoplasma sp. are generally refractory to treatment, different from S. agalactiae mastitis which is very susceptible to antibiotic treatment. As a result, S. agalactiae mastitis has been virtually eliminated, whereas mastitis caused by the other contagious mastitis pathogens continue to plague the dairy industry.

The environmental mastitis pathogens have as their reservoirs several points in the environment. Generally, the bedding is a critical reservoir involved in the transmission of mastitis. The bedding material is often organic, moist, and well seeded with bacteria and nutrients from slurry and urine. It has been established that the likelihood of an increase in environmental mastitis correlates with the bacterial load in the bedding. Added moisture with inclement weather and exposed loafing areas can lead to an increase in environmental bacterial numbers in the bedding and hence to mastitis.

An understanding of the reservoirs and the fomites of infection are important in understanding the control of mastitis and the associated pathogens. Contagious pathogens are principally transmitted during the milking process. Thus milking time hygiene, which removes the fomites of infection, can significantly reduce contagious mastitis. These techniques are: use of rubber type gloves by milkers, single service towels to wash and dry udders, use of premilking wash with disinfectant, and milking unit interior cleaning, backflush, between cow milkings. Post-milking teat disinfection, teat dipping, is possibly the single most effective means to control contagious mastitis. A high concentration of disinfectant, 10,000 ppm iodine equivalent, when applied to the teat can effectively kill residual mastitis pathogens that may have been transmitted during the milking time and thus prevent colonization of the mammary gland. The opportunistic bacteria are normal teat skin flora, and thus although teat dip reduces skin numbers, it will not eliminate transmission of these pathogens to the internal mucosal surfaces. For environmental mastitis, control can be achieved principally by keeping the environment as clean and dry as possible. Bedding should be replaced as often as needed. The replacement schedule can be a function of bedding type (organic needs more frequent removal than inorganic), weather (hot humid conditions may help promote bacterial growth, while cold and windy periods may force cows to hunker down in their stalls more frequently, as examples), and stall use, housing density and the stall’s or bedding area’s exposure to the weather.

Susceptibility to infection

Although mastitis of any form can occur at any time, some periods are more likely to be associated with mastitis at different times than others. The contagious pathogens can cause mastitis, or an outbreak of mastitis, at any time. Often in herds with excellent control programs there will be sporadic cases of contagious mastitis. The new cases are generally confined to one or a few animals and this type of mastitis will leave when the cow leaves the herd. But if a breakdown in the contagious control program occurs, or a tax on the program is made due to introduction of a new and/or virulent strain of this pathogen by introduction into the herd by purchased animal or otherwise novel introduction, then prevalence will steadily increase. The opportunistic pathogens can cause mastitis at any time. But generally they are highest at the end of the dry period, and decrease with time of lactation. Presumably these infections are of short duration and subject to spontaneous recovery. The period of greatest prevalence of environmental streptococcal IMI is the early and late dry period. In contrast, the coliforms will most likely cause IMI during the periparturient period. But again, outbreaks of environmental mastitis pathogens associated with conditions that expose the teat end to the greatest number of organisms can result in outbreaks.

Therapy

Antibiotic therapy is part of a mastitis control program. But during lactation, use of antibiotic therapy signifies the failure to have controlled the disease. Loss of monies due to the discard of antibiotic laden milk and extra labor associated with treatment and care of treated animals, will contribute significantly to loss in profit from treating lactating animals. Therefore treating subclinical mastitis infections is rarely advised. Treating clinical mastitis infections is required by the Pasteurized Milk Ordinance, and highly recommended by most mastitis experts that this author has encountered. The time to treat subclinical mastitis infections is during the dry period. During the dry period milk withholding times are not an issue, and given the length of the dry period, a longer acting, more potent formulation, of antibiotic can be used. Dry cow therapy is effective in reducing mastitis infections and will also provide some prophylactic effect.

Diagnosis

Mastitis can be monitored several ways. The most obvious is via the aseptic collection and culture of a milk sample. Examination of the mastitis pathogens in this sample will surely reveal the causative agent, but will not inform the sampler of the degree of inflammation. Moreover, the cost and care in collecting and maintaining an aseptic sample, and the non-automation of cultural methods, make this process time consuming and expensive. Thus a more prevalent monitor of mastitis is the collection of milk samples for leukocyte analysis. Samples can be preserved and inflammation is readily understood. This is a relatively inexpensive mechanism for detection of mastitis. Yet this technique suffers from the lack of knowledge of the causative agent results will reveal. Thus leukocyte analysis can be a screen for the collection of samples for culture analysis. Only those animals suspected of having mastitis as determined by leukocyte analysis can be selected for culture analysis. Leukocyte analysis is routinely done at laboratories with automated cell counters, but can be done indirectly using the California Mastitis Test, CMT. There are other automated but lesser used techniques for the monitor of mastitis. They would include: conductivity testing, lactose analysis, enzyme analysis, and protein analysis. Whereas the previous description covered the monitoring of individual cows, the herd mastitis level can be monitored by taking milk samples from the bulk tank.

The Pasteurized Milk Ordinance, the governing unit for the shipment and sale of milk, has set a limit on the number of milk somatic cells, milk leukocyte count, that is legal. That limit is currently 750,000. The PMO does therefore address mastitis as a milk quality issue. Additionally, the PMO sets requirements on the bacterial content of milk. Generally the bacterial content of milk is influenced by cleanliness of the milking system, and perhaps the cows, but is not related to mastitis. Some exceptions apply.