Developing Strategies to Reduce Mastitis
Caused by Environmental Streptococci

Ann Godkin
Ontario Ministry of Agriculture, Food and Rural Affairs
Fergus, Ontario, Canada


Contagious mastitis has been successfully controlled by herds implementing the Five Point Plan of the National Mastitis Council. This program has not proven effective against intramammary infections (IMI) caused by environmental streptococci and coliforms. A new approach is needed.

Methods of diagnosing, treating and preventing IMI caused by Streptococcus agalactiae have been well established by research and field experience. Similarly, although a more complicated disease, much is known about Staphylococcus aureus mastitis. Procedures such as post-milking teat disinfection and antibiotic treatment of all cows at the end of lactation, can be confidently recommended to producers to control these pathogens. They have been shown to produce consistent results in a wide variety of herd situations, provided they are correctly and completely implemented. Failure to keep mastitis caused by these two pathogens at an acceptable level is often a surrogate measure of the herd manager's skill and dedication, rather than a failure of the recommended control program.

Environmental mastitis, IMI with environmental streptococci (ES) and coliform bacteria, has proven to be more complex and frustrating. Producers have implemented traditional mastitis control programs yet their herds have continued to have new mastitis infections. Frequently these IMI are clinical, appearing to the herd owner to reflect an increased problem with mastitis even though herd and cow SCCs are low. Diagnosing the bacterial cause of mastitis in these types of herds can be difficult as ES and E. coli IMI are often of short duration. Negative milk culture results from cows with obvious clinical signs of mastitis can be common. Appropriate samples are often difficult to obtain. Ultimately, the recommendations made are tentative, and objective assessment of their impact is difficult to conduct.

Researchers and herd advisors have sought recommendations, as explicit as those in the 5 point plan for contagious mastitis, to prevent and treat environmental mastitis. However, because of the complexity of the factors that interact to cause environmental mastitis, it is unlikely that specific procedures that work under all conditions can be generated. Instead, it may be more appropriate to develop a standard problem-solving approach for herd mastitis problems associated with ES.

Herds with mastitis problems caused by ES seek help for two main reasons. A persistently elevated bulk milk SCC may be a problem because of the owner's desire to reduce mastitis, or because regulatory limits are exceeded. An increased rate of clinical cases will more likely be detected as herds improve record keeping and use herd management software to monitor rates of disease. The clinical case rate may be perceived as too high in comparison to the herd owner's desires for performance or to some benchmark derived from regionally collected data.

In either situation, it is necessary to have a standardized approach which can be applied to any herd. The application of basic epidemiological diagnostic principles, using clinical observations, laboratory data and information gathered from records and on-farm investigation may prove useful.

According to Schwabe the basic epidemiological diagnostic procedure is a:

"measurement of frequency and patterns of occurrence of diseases and their possible determinants, with analysis for probabilities of causal associations." (11)

Epidemiologic diagnosis can be simplified by answering the questions described below, using all available information about the problem. Information to collect includes:

What is the mastitis problem?

Clinical case records and individual cow SCCs are used to describe the mastitis problem as predominantly clinical or subclinical. A milk sampling protocol, appropriate for the type and prevalence of the mastitis problem suspected, is designed. The historical rate of new mastitis cases is used to estimate the time period for sample collection. Milk samples from affected cows are submitted to the diagnostic laboratory for bacterial culture.

Collection of composite samples from the entire herd at one time is appropriate if a large proportion of the herd has elevated SCCs on a single monthly DHI test. If only a few animals have persistently elevated SCCs then only these animals should be sampled. All clinical cases should be sampled. Milk samples from clinical quarters should be frozen until a number are collected to reduce laboratory and transportation costs.

Mastitis infections caused by ES can be of very short or very long duration. In one herd 36% lasted less than 10 days, 59% lasted less than 30 days and the geometric mean of days infected was 17 (12). In another herd researchers found the average duration of a clinical mastitis case to be 6.6 days (8). Frequently, herds affected by ES have "spiking" individual cow SCCs or report high clinical case treatment rates even though cow SCCs are rarely elevated on the monthly DHI test. This occurs because monthly SCC tests detect only a portion of short duration mastitis cases. To maximize the diagnostic sensitivity of milk culture, samples from clinical cases must be collected as soon as clinical signs are noticed. Sampling based on monthly SCCs in ES herds results in many false negative results as the timing of SCC testing will not necessarily coincide with peak bacterial numbers in all cow infections.

The equation "Prevalence = Incidence x Duration" is useful in describing dynamics of ES infections (7). This relationship indicates that the number of mastitis cases in the herd at one point in time (prevalence) depends on how many new infections occur (incidence) and how long they last (duration).

ES mastitis problems can be categorized as either high prevalence or high incidence using information from SCC, clinical case and culture records. In high prevalence herds the new infection rate is relatively low but the infections that occur are of long duration, resulting in an accumulation of infected cows in the herd. High prevalence ES herds may have continuously elevated bulk milk SCCs like those typical of herds with a high prevalence of contagious mastitis. Examination of the herd at a single time point may be sufficient to describe this high prevalence pattern of disease.

In high incidence herds many cows become infected over a given time period, but because infections are of short duration, only a few are infected on any given day. Continuous monitoring by frequent SCCs, culture, or more practically, the recording of clinical cases, is needed to accurately describe herds with this high incidence disease pattern

In some cases high incidence herds may on initial inspection, be misclassified as high prevalence herds. In these situations individual cow monthly SCCs are continuously elevated suggesting chronic infection. It is important to remember that DHI SCCs are composite samples and therefore give no information about the number or identity of high SCC quarters. Closer examination of selected cows is needed to determine whether one quarter is persistently infected or if many infections are occurring repeatedly in different quarters.

High incidence herds may have high, low or fluctuating bulk milk SCCs depending on the timing of the bulk milk sampling in relationship to the number of cows infected on that particular day. Fluctuations, particularly in small herds tested monthly can be marked. Monthly bulk milk and cow SCCs are inadequate for quantifying and monitoring ES mastitis (5). More frequent SCC determinations give a better indication of the number of cows infected (15).

Categorizing the pattern of ES mastitis as either high prevalence or high incidence must be done early in the herd investigation. Ultimately it will determine whether recommendations emphasize shortening the duration of infection, in high prevalence herds, or reducing the new infection rate, in high incidence herds.

Which individuals have mastitis?

Individual cow SCCs and clinical case records are used to identify affected animals. The frequency of cases among animals of different parity and different stages of lactation is tabulated.

Case counts by lactation number help to identify management practises that differ among age cohorts. For example, precalving environments, nutritional programs and therapy usually differ between heifers and cows and may influence the risk of mastitis. Other age differences also occur. Older cows, because of increased size, and longer lifetime exposure to the lactating cow environment, may be more prone to teat injury and milk leakage. It has been suggested that cows leaking milk at dry off time have a four times greater risk of a clinical case of mastitis during the dry period. (10). Different mastitis rates in different parity groups also can reflect historic differences in housing, bedding, therapy or milking systems.

The case rate by stage of lactation is tabulated to assess the impact of the lactating, dry cow and calving environments and management. Emphasis should be place on estimating the impact of the dry period on new ES IMI. In one detailed herd study, about half of all ES infections occurred in the first 76 days of lactation, and about half of these originated in the dry period (12). In another closely monitored herd, 87% of new IMI occurred in the dry period or within the first 7 days after calving (4). If new IMI cases occur throughout lactation then factors relating to the environment and management of lactating cows should be examined. The clustering of new IMI during lactation may point towards specific environment and management risk factors.

The earliest cow SCC test that can reliably be used to identify mastitis, is generally reported more than 15 days post-calving (1). The result of this test gives little information about IMI occurring during the peri-parturient period, a time of high risk for ES infections. Case recording by the producer is essential to identify housing or management factors that increase the risk of mastitis at this time. Additional tests, such as the California Mastitis Test (CMT), can be used to collect specific data on mastitis rates during this time period.

When and where is mastitis occurring?

Records of clinical cases and SCCs can be used to determine where on the farm or in the housing system cows are most at risk of new ES IMI. On-farm investigation and careful observation can detect factors likely to be associated with mastitis.

Both external and internal farm climates can affect ES mastitis. Unfortunately few quantitative studies exist examining this impact on ES mastitis rates. Seasonal changes in temperature and humidity, have been shown to affect the rate of ES and clinical mastitis (4,9,12). Annual periods of high risk can be determined by examining the rate of new ES or clinical mastitis infections that occur monthly. Recognition of these times can lead to the development of proactive strategies to moderate this effect.

Examination of areas on the farm associated with an increased rate of new ES IMI will identify internal farm climates that lead to problems. Uneven calving rates, the birth of a high proportion of heifers, or low production are examples of changes that can temporarily increase the animal density within certain environments. Producers often fail to recognize the potential impact of these changes on environmental bacterial numbers and exposure of the herd to an increased risk of ES mastitis.

Proper housing management should reduce the concentration and multiplication of ES in the environment. Improved ventilation can reduce temperature and humidity. Bedding hygiene and types also have been shown to impact on ES mastitis (6,12). Differences in mastitis rates between milking groups, certain housing areas, stalls of differing dimensions or associated with different milking personnel may be found. Closer examination of factors associated with the problem location is warranted. Sometimes the final cause of mastitis is not found but a solution to the problem becomes obvious.

What "caused" the mastitis problem?

ES in the cow's environment is a necessary cause of ES mastitis but the presence of the bacteria does not always cause mastitis. A variety of other factors which affect bacterial numbers in the environment, exposure of the teat end and the resistance of the cow are also important. Intervention to prevent ES mastitis involves manipulation of one or more of these component causes.

Why did mastitis occur?

Clinical case records, laboratory and other testing data are analyzed to define the problem as described above. A simple hypothesis about why mastitis is occurring is generated. If herd size and case numbers are large enough factors suspected of contributing to the problem can be statistically tested to verify their relationship to mastitis. Formal evaluation establishes that the difference observed is unlikely to have occurred due to chance alone.

How is the mastitis problem controlled or prevented?

Once factors suspected of causing ES mastitis are identified, recommendations are made to provide solutions. They must be specific to the current problem, few in number and clearly explained to maximize compliance. Recommendations are ranked in priority based on the overall importance attributed to changing that factor and on the ease and timeliness with which the change can be made.

Often there will be short and long term recommendations. For example, if new IMI's are occurring at calving time, it may be recommended to calve cows temporarily in a driving shed or outside on pasture. The long term recommendation would be to increase the number of maternity pens to accommodate the maximum number of expected calvings.

In high prevalence herds, shortening the duration of existing infections is emphasized. If the bulk milk SCC is close to penalty levels treating affected lactating cows identified from SCC and culture reports would be critical. Drying cows off prematurely and treating with dry cow antibiotic products could also help, if economics allowed their removal from the bulk tank. In less pressing situations ensuring all cows receive dry cow antibiotic treatment at the end of lactation will cure 84 to 100 % of ES infections (2,4) and reduce the prevalence at the following calving (12,14).

In high incidence herds strong emphasis is placed on recommendations which reduce the new IMI rate. These recommendations are highly herd and situation specific. Lactational and dry cow treatment with antibiotic may be of little use in these herds. As rapidly as existing infections are removed, new ones start.

To evaluate the effectiveness of the changes recommended appropriate monitoring measures should be selected. For example, if dry cow treatment is implemented, data on clinical cases and CMT evaluations post-calving, should be collected started with cows calving two months after the new treatment is implemented. The evaluation should continue until enough cows have calved to prove the usefulness of the change.

Summary

Traditional mastitis monitoring and control programs have focused on contagious mastitis. However, as the prevalence of contagious pathogens in many jurisdictions declines, ES mastitis is assuming greater importance. Strategies for ES mastitis prevention, that work in concert with current housing and management systems, have yet to be developed and tested in field situations.

Epidemiological diagnosis using the questions described above, offers a logical and rational process for the investigation of herd ES problems. Ultimately, herd specific solutions are created. Producer compliance is maximized because these programs relate to the individual's herd, farm environment and the current problem.

References

 1. Dohoo IR, AH Meek. 1982. Somatic cell counts in bovine milk. Can Vet J 23:119.

 2. Bramley AJ. 1984. Streptococcus uberis udder infection--a major barrier to reducing mastitis incidence. Br Vet J 140:328.

 3. Erskine RJ, RJ Eberhart. 1987. Comparison of duplicate and single quarter milk samples for the identification of intramammary infections. J Dairy Sci 71:854.

 4. Hillerton JE, AJ Bramley, RT Staker, CH McKinnon. 1995. Patterns of intramammary infection and clinical mastitis over a five year period in a closely monitored herd applying mastitis control measures. J Dairy Res 62:39.

 5. Hogan JS, KH Hoblet, KL Smith, DA Todhunter, PS Schoenberger, WD Hueston, DE Pritchard, GL Bowman, LE Heider, BL Brockett, HR Conrad. 1988. Bacterial and somatic cell counts in bulk tank milk from nine well managed herds. J Food Prot 51:930.

 6. King JS. 1981. Streptococcus uberis: A review of it's role as a causative organism of bovine mastitis. I: Characteristics of the organism. Br Vet J 137:36.

 7. Martin SW, AH Meek, P Willeberg. 1987. Veterinary epidemiology: Principles and methods. Iowa State University Press, Ames, Iowa.

 8. Morse D, MA DeLorenzo, RP Natzke, DR Bray. 1982. Factors affecting days of discarded milk due to clinical mastitis and subsequent costs of discarded milk. J Dairy Sci 70:2411.

 9. Morse D, MA DeLorenzo, CJ Wilcox, RJ Collier, RP Natzke, DR Bray. 1988. Climatic effects on occurrence of clinical mastitis. J Dairy Sci 71:848.

10. Schukken YH, J VanVliet, D Vandegeer, FJ Grommers. 1993. A randomized blind trial on dry cow antibiotic infusion in a low somatic cell count herd. J Dairy Sci 76:2925.

11. Schwabe CW. 1984. Veterinary medicine and human health. Williams & Wilkins, 428 East Preston Street, Baltimore, MD. 393.

12. Smith KL, DA Todhunter, PS Schoenberger. 1985. Environmental mastitis: cause, prevalence and prevention. J Dairy Sci 68:1531.

13. White ME, M Montgomery. 1987. The resemblance of clinical mastitis attributes between mastitis cows with no growth on bacterial milk cultures and those with gram-positive bacteria cultured. Can J Vet Res 51:181.

14. Williamson JH, Woolford M, AM Day. 1995. The prophylactic effect of a dry-cow antibiotic against Streptococcus uberis. N Z Vet J 43:228.

15.  Woolford M. 1997. Proceedings of the 36th Annual Meeting of the National Mastitis Council. 56.

(From Proceedings of the Symposium "Udder Health Management for Environmental Streptococci", June 22, 1997, Guelph, Ontario, pg. 87)


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