Milk quality issues

Department of Animal Sciences, University of Kentucky, Lexington, KY, USA


Introduction

Somatic cell counts (SCC) are readily available to every dairy farmer in the United States on a monthly basis and to farmers in most of the developed countries. Somatic cell counts are accepted as the international standard measurement of milk quality and, for this reason, are rapidly being made available in developing countries where they have not previously been utilized. Extensive data are now available worldwide on large numbers of cows concerning factors affecting SCC in milk.

Comparing these SCC data with bacteriological culture results gives a reasonable idea which factors are of greatest importance in affecting SCC levels and may clarify some misconceptions concerning changes in SCC. The basic fact is that intramammary infections are the major factor affecting SCC at the quarter, cow, or bulk tank level and no other factor will dramatically increase its level. If a dairy farmer is effective in preventing new infections (mastitis) and removes chronic cases from the herd, the herd SCC can be decreased to 100,000 or lower.

General mastitis control

Mastitis continues to be the most costly disease problem in the dairy industry. Control of the contagious pathogens Staphylococcus aureus and Streptococcus agalactiae through effective programs of milking hygiene, dry cow therapy, postmilking use of germicidal teat dips and culling chronic cows has resulted in the eradication of S. agalactiae from many dairy herds and markedly reduced incidence of S. aureus. However, herds which have effectively controlled contagious pathogens and routinely produce milk of high quality with low bulk tank somatic cell counts may still suffer losses due to infections by environmental mastitis pathogens. In addition, such herds may experience seasonal or management-related outbreaks that increase the bulk tank somatic cell count accompanied by increased incidence of clinical cases. Since the reservoirs for the environmental pathogens include soil, feces and bedding, cattle are constantly exposed to these organisms at some level, and no single control procedure seems to be effective for all environmental organisms. However, some management approaches and new developments in enhancing disease resistance may provide progress toward controlling this disease complex.

Environmental pathogens

It is important to understand the complexity of environmental mastitis before addressing the question of control. The environmental mastitis pathogens are the coliforms, streptococci other than S. agalactiae and the enterococci. The common coliforms associated with mastitis are Escherichia coli, Klebsiella spp. and Enterobacter aerogenes. The environmental streptococci include Streptococcus uberis, Streptococcus dysgalactiae and Streptococcus bovis. Enterococcus faecium and Enterococcus faecalis are the common enterococci. One difference between contagious and environmental pathogens is that the primary reservoir for contagious pathogens is the infected udder and exposure is during milking. In contrast, the environmental pathogens survive and multiply readily in extra-mammary sites, especially bedding, and the exposure to these organisms usually occurs between milkings (Hogan and Smith, 1987).

MASTITIS DUE TO ENVIRONMENTAL STREPTOCOCCI

The rate of new intramammary infection (IMI) is higher in the dry period than during the lactation. New infection rate is highest during the first two weeks of the dry period and again during the two weeks before parturition. Rate of new IMI is also greater in early lactation than during the remainder of lactation. Approximately 60% of infections by environmental streptococci last less than 30 days and about 18% last more than 100 days. Approximately 50% of infections by environmental streptococci cause clinical mastitis. The percentage of mammary quarters in a dairy herd infected with these environmental organisms at any particular time (i.e. prevalence) tends to be low and is generally less than 10% for the total of all environmental organisms (Smith et al., 1985a; Hogan and Smith, 1987).

COLIFORM MASTITIS

Rate of new IMI is about four times higher in the dry period than during lactation, and the rate is greatest during the first two weeks of the dry period and the two weeks before parturition. During lactation the rate of IMI is highest in early lactation and decreases as lactation progresses. Duration of coliform infections tends to be short; 57% of infections last less than 10 days and 69% are less than 30 days in length. In about 13% of cases the duration is greater than 100 days. A high percentage of coliform infections during lactation result in clinical mastitis (80 to 90%).

However, only 8 to 10% result in peracute or ‘toxic’ cases. It is not unusual for E. coli to be eliminated from the udder by phagocytic cells by the time clinical signs are apparent. Thus, the bacteriological culture of clinical milk samples may naturally result in some proportion that are negative (no growth).

RISK FACTORS FOR ENVIRONMENTAL MASTITIS

It is now accepted that the most common mastitis problems in herds with low bulk tank somatic cell counts (i.e. have controlled contagious pathogens) is clinical mastitis due to environmental pathogens. There are a variety of factors that determine the new infection rate or rate of clinical mastitis by these pathogens.

Housing

It is a general observation that housed cattle are at greater risk of environmental mastitis than cattle on pasture (Hogan and Smith, 1987). An interesting study by Meaney (1981) compared major pathogen prevalence at calving in heifers that were housed or reared on pasture. The quarter infection prevalence at calving was 2.4-fold higher in housed heifers (18.8%) compared with that in pastured heifers (8%). Seventy percent of infections or clinical cases in the pastured heifers and 98% in housed heifers were by environmental pathogens or no pathogen was isolated.

Situations that increase cow density may contribute to increased environmental pathogen load, even in pastures. The congregation of cattle around shaded areas in pastures during hot summer months resulted in environmental pathogen numbers exceeding 10 million per g dry matter in the soil (Harmon et al., 1992). These levels were as high as that observed in soiled sawdust in free stalls.

Bedding

Bedding materials are a significant source of environmental pathogens. Organic materials such as straw, shavings and sawdust have been shown to support higher numbers of environmental bacteria than inorganic materials such as sand or limestone (Hogan and Smith, 1987; Hogan et al., 1989b). In addition, increased ambient temperature and moisture tend to enhance growth of pathogens.

Coliform counts were highest in summer and fall. Klebsiella spp. counts were higher in sawdust than in chopped straw, and streptococcal counts were higher in straw than in sawdust. Hogan et al. (1989b) reported a significant linear relationship between total rates of clinical mastitis during lactation and Gram-negative bacterial and Klebsiella spp. counts in bedding. Thus, there is an apparent relationship between level of exposure and new infection rate or clinical incidence of mastitis.

Season

Hogan et al. (1989a) studied the rates of clinical mastitis in nine well-managed, low somatic cell count herds. Environmental pathogens and bacteriologically negative samples accounted for 82.3% of clinical cases. Only 4.9% of bacteriologically positive samples were from contagious pathogens. They found that clinical cases were highest in summer and fall. This compares with a previous three-year study showing high frequencies of IMI and clinical cases in summer months caused by environmental pathogens (Smith et al., 1985a).

ENVIRONMENTAL MASTITIS IN HEIFERS

Since it is recognized that cows are at increased risk of new IMI by environmental pathogens early in the dry period and in the peripartum period, it would be logical to assume that the primiparous cow at or near parturition would likewise be at higher risk to new infections under similar exposure.

It is not unusual in modern herds to find 5 to 10% of quarters in heifers at calving infected with environmental pathogens. This would be observed as increased SCC in early lactation and increased incidence of clinical mastitis. In the study by Meaney (1981) the infection prevalence at calving was 2.4-fold higher in housed heifers (18.8%) compared with that in pastured heifers (8%).

These studies of environmental pathogen prevalence in primiparous cows are in agreement with the streptococci (3.3% of quarters) and coliform (3.5% of quarters) infection prevalence of cows at calving reported by Smith et al. (1985a). These workers reported an increase in rate of IMI by environmental pathogens with parity in one herd over three years. In contrast, a survey of nine commercial dairy herds revealed the rates of clinical mastitis were highest in first lactation cows (Hogan et al., 1989a). Coliforms, bacteriologically negative, and environmental streptococci accounted for 82.3% of clinical cases. Despite this disagreement in results, it would appear that primiparous cows in herds that have controlled contagious mastitis can still be at considerable risk to new IMI by environmental pathogens in the peripartum period (Harmon, 1990).

ECONOMIC LOSSES

The estimated economic losses due to clinical mastitis in low somatic cell count herds has been documented (Hoblet et al., 1991). Total costs per clinical episode were estimated to be $107 (range, $46 to 142). Eighty-four percent of the losses were due to decreased milk production and non-salable milk. Hoblet et al. (1991) reported an average of 38% of lactations in one year experienced clinical episodes with a 4-fold range (16 to 64%) of clinical incidence among nine herds. It again should be stressed that these were well-managed commercial herds that had controlled contagious mastitis pathogens.

CONTROL OF ENVIRONMENTAL MASTITIS

The approaches to the control of environmental mastitis must involve prevention by either decreased exposure to pathogens or enhanced resistance of the dairy cow. Unfortunately, many procedures that effectively control contagious mastitis have limited or no efficacy against environmental pathogens (Crist and Harmon, 1991).

Teat dipping and dry cow therapy

Basic mastitis control programs should include postmilking teat dipping and dry cow therapy with antibiotics. In general, teat dipping with germicidal dips has no efficacy against coliforms and limited efficacy against environmental streptococci. Of the environmental streptococci S. dysgalactiae seems to be controlled more readily by milking time hygiene. The limited efficacy of post-milking teat dipping against environmental pathogens likely is related to the exposure between milkings and after dip has been applied. Dry cow therapy reduces new streptococcal IMI early in the dry period but has limited value against coliforms.

Barrier teat dips

Although post-milking barrier teat dips have been reported to reduce new coliform infections, their efficacy against streptococcal infections is less than that of germicidal dips. Teat dipping with traditional germicidal or barrier teat dips (designed for lactating cows) in the dry period has not been successful in preventing environmental mastitis. However, new formulations that provide a more long-lasting physical barrier, designed for the dry cow, show some promise.

Milking procedures

General hygiene in the milking process should always be followed. Milking wet teats may increase new environmental pathogen infections. Anything that causes liner slippage may increase new infections. Teats should be clean and dry before machine attachment and equipment must be in good working order.

Predipping

Predipping, i.e. use of germicidal teat dip before milking, has been shown to reduce environmental mastitis by 50% (Pankey et al., 1987). However, complete drying of teats after application is critical to prevent residues in milk. The success of this procedure may vary greatly from herd to herd.

Environment

There is no single method or product to reduce exposure in the environment. The key principles are clean and dry environment and require good management. This applies to lactating cows, heifers and cows during the dry period. Daily removal of manure from concrete areas is recommended. The daily removal of soiled sawdust bedding from the rear meter of free stalls and replacement with fresh sawdust resulted in reduction of coliform numbers from 100 million per g to approximately 1million per g (Dodd et al., 1984). This resulted in an apparent 90% reduction in clinical coliform cases. Housing cows on sand resulted in a 4-fold lower incidence of clinical coliform mastitis compared with sawdust. Prevention of cows from congregating in certain areas of pastures may reduce pathogen load. The use of portable shades that can be moved frequently may reduce manure buildup and pathogen exposure in hot weather. Ponds and shade trees should be fenced off to limit access to mud and contaminated water. Access to grassy lots and the rotation of animals between several pastures may help to maintain the sod and keep animals cleaner.

ENHANCED RESISTANCE

Several approaches have been investigated to enhance the resistance of the mammary gland to new infection or reduce clinical severity of the disease. These aproaches should serve a supplemental role to sound nutrition and management and not as their replacement or a ‘quick fix’.

Vaccines

Although previous research on ‘mastitis vaccines’ has met with limited if any success in controlling the disease, immunization studies using a J5 E. coli whole cell bacterin has shown success (Cullor, 1991). Field studies in commercial dairies have demonstrated that the bacterin is safe and efficacious. The incidence of clinical coliform mastitis was approximately 70% less in vaccinated cows compared with those receiving placebo or unvaccinated controls. In addition, vaccinated cows experienced a reduced rate of recurrent infections. Several vaccines against coliforms are available today and are widely used to reduce clinical coliform mastitis at calving. However, successful immunization will remain a useful tool in the control of mastitis and must be only a part of the total management scheme.

Nutrition

The increased interest and research effort in the area of nutritional relationships to host defense has encouraged new and potentially beneficial approaches for enhancing resistance of the dairy cow to intramammary infection by major mastitis pathogens or limiting the severity of response to invasion of the mammary gland when it does occur. Particular emphasis has been made on proper micronutrient nutrition in the dry period, because the time of drying off and the periparturient period are the times when the mammary gland is most susceptible to new infections by the environmental pathogens.

Deficiencies in dietary selenium and vitamin E have been shown to result in increased incidence of mastitis. Supplemental dietary Se and vitamin E were shown to lower the frequency and shorten the duration of clinical mastitis (Smith et al., 1984). A later Ohio study (Smith et al., 1985b) evaluated mastitis incidence in heifers either supplemented with vitamin E and Se or those receiving no supplemental vitamin E and Se from 60 days prepartum and throughout lactation. Prepartum dietary supplementation was with approximately 1000 IU vitamin E per head per day and 2 mg Se per head per day. In addition, supplemented heifers received a subcutaneous injection of Se (sodium selenite) at 21 days prepartum. Lactation supplementation was 600 to 800 IU vitamin E and 2 mg Se per head per day. Vitamin E and Se supplementation resulted in:

1. 42% reduction in prevalence of infection at calving.
2. 57% reduction in clinical mastitis in early lactation and 32% reduction throughout lactation.
3. 40 to 50% reduction in duration of infections.
4. Significantly lower somatic cell counts for the lactation.

Overall, vitamin E and Se improved udder health, and the effect was most evident at calving and early lactation.

Another area of micronutrient nutrition that shows potential in this regard is the influence of copper and zinc status on host defense and mastitis. Further, supplementation with copper and zinc proteinates shows promise in improving udder health and somatic cell counts. The reduction in mastitis and lowering somatic cell counts in a dairy herd will result in significant economic benefits as well as improved welfare of the cattle.

References

Crist, W.L. and R.J. Harmon. 1991. Controlling mastitis - The problem, its impact and future perspectives. In: Biotechnology in the Feed Industry: Proceedings of Alltech’s 7th Annual Symposium (T.P. Lyons, ed), Alltech Technical Publications, Nicholasville, KY, pp. 265-276.

Cullor, J.S. 1991. The role of vaccines in prevention and moderation of clinical mastitis. Proc. 30th Ann. Mtg. Natl. Mastitis Counc., Natl. Mastitis Counc., Arlington, VA, pp. 68-75.

Dodd, F.H., T.M. Higgs and A.J. Bramley. 1984. Cubicle management and coliform mastitis. Vet. Record 114:522-523.

Harmon, R.J. 1990. Intramammary infections in primiparous cows in the periparturient period. Proc. 29th Ann. Mtg. Natl. Mastitis Counc., Natl. Mastitis Counc., Arlington, VA, pp. 44-57.

Harmon, R.J., T. Clark, T. Ramesh, W.L. Crist, B.E. Langlois, K. Akers and B. Smith. 1992. Environmental pathogen numbers in pastures and bedding of dairy cattle. J. Dairy Sci. 75(Suppl. 1):256.

Hoblet, K.H., G.D. Schnitkey, D. Arbaugh, J.S. Hogan, K.L. Smith, P.S. Schoenberger, D.A. Todhunter, W.D. Hueston, D.E. Pritchard, G.L. Bowman, L.E. Heider, B.L. Brockett and H.R. Conrad. 1991. Costs associated with selected preventive practices and with episodes of clinical mastitis in nine herds with low somatic cell counts. J. Am. Vet. Med. Assoc. 199:190-196.

Hogan, J.S. and K.L. Smith. 1987. A practical look at environmental mastitis. Compendium on Continuing Education for the Practicing Veterinarian 9(10):F341-346.

Hogan, J.S., K.L. Smith, K.H. Hoblet, P.S. Schoenberger, D.A. Todhunter, W.D. Hueston, D.E. Pritchard, G.L. Bowman, L.E. Heider, B.L. Brockett and H.R. Conrad. 1989a. Field survey of clinical mastitis in low somatic cell count herds. J. Dairy Sci. 72:1547-1556.

Hogan, J.S., K.L. Smith, K.H. Hoblet, D.A. Todhunter, P.S. Schoenberger, W.D. Hueston, D.E. Pritchard, G.L. Bowman, L.E. Heider, B.L. Brockett and H.R. Conrad. 1989b. Bacterial counts in bedding materials used in nine commercial dairies. J. Dairy Sci. 72:250-258.

Meaney, W.J. 1981. Mastitis levels in spring-calving dairy heifers. Irish Vet. J. 35:205-209.

Pankey, J.W., E.E. Wildman, P.A. Drechsler and J.S. Hogan. 1987. Field trial evaluation of premilking teat disinfection. J. Dairy Sci. 70:867- 872.

Smith, K.L., J.H. Harrison, D.D. Hancock, D.A. Todhunter and H.R. Conrad. 1984. Effect of vitamin E and selenium supplementation on incidence of clinical mastitis and duration of clinical symptoms. J. Dairy Sci. 67:1293-1300.

Smith, K.L., D.A. Todhunter and P.S. Schoenberger. 1985a. Environmental mastitis: cause, prevalence, prevention. J. Dairy Sci. 68:1531-1553.

Smith, K.L., H. R. Conrad, B.A. Amiet and D.A. Todhunter. 1985b. Incidence of environmental mastitis as influenced by dietary vitamin E and selenium. Kieler lchwirtschaftliche Forschungsberichte 37:482.