- Email: [email protected]
Managing Environmental Mastitis
Managing Environmental Mastitis Joe Hogan, PhD*, K. Larry Smith, PhD
KEYWORDS • Mastitis • Bedding • Dairy cows • Intramammary infections KEY POINTS • Coliform bacteria, streptococci, and enterococci are the most common etiologic agents of environmental mastitis. • The primary agents of environmental mastitis are of fecal origin but can also heavily contaminate organic materials such as bedding, feed, and soil in the cows’ surroundings. • Washed sand contains 100-fold fewer mastitis pathogens per gram of bedding compared with common organic bedding materials. • Management keys to reducing exposure of cows to environmental mastitis pathogens include frequent manure removal, eliminating standing water in the cow’s walking lanes and loafing areas, and avoiding overcrowding of animals in barns and pastures. • Populations of mastitis pathogens increase in the cow’s environment as ambient temperature and moisture increases. • Rates of environmental mastitis are greatest during the dry period and early lactation compared with other stages of lactation.
The most common environmental mastitis pathogens among herds of North America are those grouped as coliforms and environmental streptococci. The term “coliform mastitis” frequently is used incorrectly to identify mammary disease caused by all gram-negative bacteria.1 Genera classified as coliforms are Escherichia, Klebsiella, and Enterobacter. Other gram-negative bacteria frequently isolated from intramammary infections include species of Serratia, Pseudomonas, and Proteus.2 Coliform bacteria occupy many habitats in the cow’s environment. Escherichia coli are normal inhabitants of the gastrointestinal tract of warm blooded animals. Both Klebsiella spp and Enterobacter spp populate soils, grains, water, and intestinal tracts of animals. Serratia marcesens share many environmental sources with Klebsiella spp and
Salaries and research support were provided by state and federal funds appropriated to the Ohio Agricultural Research and Development Center, The Ohio State University. The authors have nothing to disclose. Ohio Agricultural Research and Development Center, The Ohio State University, Wooster, OH 44691, USA * Corresponding author. E-mail address: [email protected] Vet Clin Food Anim 28 (2012) 217–224 http://dx.doi.org/10.1016/j.cvfa.2012.03.009 vetfood.theclinics.com 0749-0720/12/$ – see front matter © 2012 Elsevier Inc. All rights reserved.
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Enterobacter spp. Pseudomonas spp and Proteus spp commonly contaminate drop hoses used to wash udders before milking. The group of bacteria collectively labeled environmental streptococci includes Streptococcus uberis, Streptococcus dysgalcatiae, and Enterococcus spp.3 The environmental streptococci, S uberis in particular, have been isolated from bedding materials, soil, rumen, feces, vulva, lips, nares, mammary gland, and teats.4,5 Feed stuffs such as silages and green chop forages may also be a source of these pathogens and infections of the reproductive tract may contribute to environmental and teat end contamination.6 STALL BEDDING IS A KEY ENVIRONMENTAL SOURCE
The key to controlling environmental mastitis to an economically acceptable level within a herd is to reduce the exposure of cows to the pathogens. Although bacteria that cause environmental mastitis are among the etiologic agents commonly responsible for infectious respiratory and urogenital diseases in dairy cows,7 the spread of these bacteria from other regions of the body to the mammary gland via the vascular or lymphatic systems appears minimal. Intramammary infections caused by environmental mastitis pathogens typically result from the bacteria traversing the teat canal and multiplying in the gland. These bacterial species are chemotropic organisms requiring organic material to use as food. Coliforms and streptococci cannot live on teat skin for long periods of time. If these bacteria are present in large numbers on teat skin, it is the result of recent contamination. Therefore, the number of these bacteria on teat skin is a reflection of the cow’s exposure to the contaminating environment.8,9 Cows lay down 12 to 14 hours a day, and their teats are in direct contact with the bedding or other materials where they rest. Populations of the bacteria in bedding are related to the number of bacteria on teat ends and rates of clinical mastitis.9,10 Therefore, reducing the number of bacteria in bedding generally results in a decrease in environmental mastitis. Coliforms cannot live on teat skin for long periods of time. If these bacteria are present in large numbers on teat skin, it is the result of recent contamination from a source such as bedding. Hygiene and proper management of stall, lots, and pastures are essential. Sand Bedding
Ideally, bedding should be inorganic materials that are low in moisture content and contain few nutrients for bacteria to use. The bedding material that we recommend most for controlling environmental mastitis is washed sand. Compared to organic materials such as sawdust, recycled manure, straw, and dirt, washed sand consistently contains 100-fold fewer mastitis pathogens per gram of bedding.10 The effectiveness of sand for reducing exposure of mastitis pathogens to mammary glands is due to the inorganic properties of sand. However, as organic content and moisture in sand bedding increase during the common practice of on-farm reclaiming sand from sand-laden manure, the mastitis pathogen populations also increase.11 A realistic goal for dry matter of sand used for bedding is greater than 95%. Organic matter in sand bedding should be less than 5%. Organic Bedding
Many farms are forced to use organic bedding materials that are compatible with liquid manure– handling systems. Little advantage exists in using one organic material over the use of another. For example, straw tends to have highest streptococcal counts, while sawdust has the highest coliform counts in comparisons among these
Managing Environmental Mastitis
bedding materials.10 Any material to be used as bedding should be stored in a dry area to prevent saturation by rain and ground moisture. Composting organic materials is an effective way to reduce bacterial counts before use as bedding. However, although many organic bedding materials have relatively few mastitis pathogens prior to use, the pathogen populations often increase 10,000-fold within hours after use as bedding.12 Fresh bedding tends to absorb moisture from the cows’ environment for use by the great number of bacteria that are constantly present in manure and soiled bedding. Organic materials used as bedding in North America have historically been affordable byproducts of the grain crops or the forestry and wood industry. Two trends have caused a shift from these organic bedding sources to the use of recycled manure solids on many dairies. First, the availability of sawdust, wood shavings, and straw has diminished with the increased of use of these products for home heating fuel and landscaping mulch. Second, the use of methane digesters on some dairies results in available solids and the profitability of digesters necessitates the use of solids for bedding. In general, bacterial counts in manure solids are similar to those in sawdust. The key to successful use of manure solids is to lower the moisture content, thus lowering the bacterial counts of mastitis pathogens. A realistic goal for manure solids when placed in stalls is 35% dry matter. Regardless of the bedding used, removing wet and soiled material from the back third of stalls will significantly reduce the bacterial counts. Stalls should be raked a minimum of twice daily when animals are moved to be milked. A practice that is often successful in herds using manure solids is the daily complete replacement of bedding in back third of stalls. Spraying bedding with disinfectant and adding powdered lime to bedding have met with little practical success in reducing bacterial counts.13 These practices cause an initial decline in bacterial populations, but pathogen numbers quickly recover. Twice-a-day application of powdered lime may be necessary to sustain an advantage in lowering bacterial numbers. Standing water and mud should be avoided in stalls, holding areas, and lots. Overcrowding of free-stall barns increases the manure contaminating the alleys and lanes. The accumulated manure in alleys will splatter on hooves and legs to contaminate bedding with organic matter and inoculate the bedding with fecal bacteria. Cows’ access to dirt-manure lots also should be limited during rainy seasons. Outbreaks of coliform mastitis are common during rainy seasons when cows are exposed to dirt-manure lots and lanes leading to the milking parlors. Seasonal Effects
Climatic factors that affect the risk to environmental mastitis are temperature and humidity. As the ambient temperature and moisture increase, populations of pathogens increase in the cow’s environment and the mammary defense systems to combat infections become compromised. Growth rates of coliforms and environmental streptococci are greatest during warm, wet weather. The effects of season on bacterial populations in bedding are quite dramatic in regions that experience a wide variation of temperatures within a year. In general, the impact of bedding on exposure of cows in confinement housing decreases during cold weather and increases as temperatures and humidity increase.10 Previous trials have shown a strong correlation between bacterial counts in bedding and both ambient temperature and relative humidity.14 Overcrowding of barns with cows will exasperate the effects of heat and humidity. Therefore, adequate ventilation of barns and proper stocking rates are essential to moderate the effects of heat and humidity in housing areas.
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Dry Lots and Corrals
Dirt and manure covered corrals are commonly used to house cows in semiarid and arid areas where temperatures are seldom below freezing for an extended time. Exposure to pathogens generally is low during the dry seasons as moisture content of the dirt-manure mixture is low. However, as density of cows increase under shade structures and around feeding areas and water troughs, excess wet organic matter should be removed or spread out to be dried.15 Climatic factors affecting exposure in herds where cows are maintained on dry lots differ from those of in-stall barns. The rainy seasons of late fall through early spring are when bacterial populations are greatest. Manure in dry lots during the summer tends to be desiccated, thus limiting the moisture essential for bacterial growth. Grazing Systems
The majority of research on the effects of grazing systems on mammary health has been conducted outside of North America. However, the overriding principle of reducing pathogen exposure by the use of grazing pastures appears universal. Grazing management systems often decrease pathogen loads in the cows’ environment compared with total confinement systems. Turf-covered soil in grazing paddocks typically have minimal contamination with environmental mastitis pathogens when compared with organic bedding in stalls or loose housing. Bacterial exposure increases as forage is closely grazed and stocking rate increases.16,17 Ample time between rotation of cows on paddocks is needed to allow forage regrowth over soil and manure load to dissipate. Barren soil due to overgrazing and trampling can harbor elevated populations in the cows’ environment.18 Areas around feed troughs, exercise lots, and lanes often expose cows to bacterial concentrations comparable to that in organic bedded stalls. Removal of wet organic matter and replacement with dry, inorganic materials will reduce exposure. Similar to dry lots, solar radiation and drying during summer months reduce bacterial contamination in these areas compared with rainy winter months.17 Maternity and Dry Cow Lots
As evidenced later in the article, the rate of new intramammary infections caused by environmental mastitis pathogens is greater during the dry period than during lactation. Management and hygiene of dry cow housing and maternity areas should be priorities. Fortunately, the management practices for reducing mastitis pathogen exposure in dry cow and maternity facilities are similar to those for lactating cow housing. Dry cow areas should be well drained and free of excess manure. Dirt-covered areas can expose cows to pathogen levels comparable to those in free-stalls. Box stalls and loose housing areas should be cleaned to the foundation base regularly. Manure packs are to be avoided because they generally contain extremely high counts of pathogens that are dangerous to both dam and calf. Milking Hygiene
Milking time hygiene is the basis for control of contagious mastitis but has less influence on environmental mastitis. The use of germicidal teat dips postmilking will have minimal effect on incidence of new intramammary infections caused by coliform or environmental streptococci. Teat dip efficacy is dependent on the time of application relative to milking and the pathogens causing mastitis. Most germicidal teat dips effectively and rapidly destroy microbes on teat skin by chemical or biological action. However, the persistency of germicidal activity is limited and
Managing Environmental Mastitis
neutralized by organic material such as milk and manure.1 Therefore, although most germicidal products will kill coliforms on teat skin, exposure to these pathogens occurs primarily between milkings, long after the killing activity of the dips has diminished. Predipping teats before milking in an effective disinfectant reduces new intramammary infections caused by coliforms during lactation. Field trials have shown predipping reduces the incidence of clinical mastitis by 50% in herds with low levels of contagious mastitis.19 Current recommendations in North America for predipping include forestripping the first few streams of milk, removing excess manure and dirt from teats, dipping teats in the germicidal teat dip, allowing teat dip to contact teat skin at least 30 seconds, and manually drying teats with either individual paper towels or freshly laundered cloth towels. Barrier dips form a physical obstruction between teat skin and the environment. Latex, acrylic, and polymer based products form a physical seal over the teat end to impede entrance into the udder between milkings. The use of some latex barrier teat dips may reduce the incidence of coliform mastitis, but the efficacy of physical barrier teat dips against other pathogens is minimal. Barrier teat dips containing germicides have not been shown to be more effective than conventional germicidal dips in reducing environmental mastitis in controlled studies.20 MONITORING CLINICAL MASTITIS
The ultimate measure of success in reducing exposure to environmental mastitis pathogens is improvement in mammary health. Bulk tank and monthly cow somatic cell counts (SCCs) are poor milk quality indicators of environmental mastitis. The prevalence of intramammary infections caused by environmental pathogens within a herd is seldom great enough to cause bulk tank SCCs of higher than 250,000/mL, but approximately 85% of coliform and 50% of environmental streptococcal infections will cause clinical mastitis. Surveys of herds with low bulk tank SCCs21 have shown the average rate of clinical mastitis to be 46 cases per year in a 100-cow herd (3.8% of cows per month). The high frequency of clinical cases and relatively short duration of these intramammary infections render the use of individual cow SCC and bulk tank SCC as poor indicators of the prevalence of disease caused by these bacteria. For example, prevalence of intramammary infections caused by environmental mastitis pathogens seldom exceeds 5% of quarters in a herd; however, 20% and 15% of cows in well-managed herds are annually diagnosed with clinical mastitis caused by coliforms and environmental streptococci, respectfully. A realistic goal for rate of total clinical cases in a well-managed herd is 2% of cows per month. The severity of clinical mastitis caused by environmental pathogens ranges from mild local signs to death. The vast majority of clinical coliform and environmental streptococcal clinical cases are characterized by only abnormal milk and a swollen gland. Only about 10% of clinical coliform cases result in systemic signs including fever, anorexia, and altered respiration.22,23 Despite the relatively low percentage of clinical coliform cases yielding systemic signs, coliform bacteria have an exaggerated reputation for causing severe mastitis. The basis for this distinction originates from the point that the coliforms are the most common cause of systemic illness resulting from mastitis. Survey averages suggest that coliform bacteria are the culprits of 60% to 70% of severe clinical cases involving systemic signs.22,23 Therefore, the general conclusions concerning severity of clinical coliform cases are that few coliform intramammary infections cause systemic clinical signs, but the majority of clinical cases resulting in systemic signs are caused by coliform bacteria. Stage of lactation has a tremendous impact on cows’ susceptibility to environmental mastitis. Recording the number of clinical cases and documenting the stage of
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lactation when they occur will aid in determining when cows are at greatest risk to clinical mastitis. Rates of new intramammary infections caused by coliforms are generally greater during the dry period than during lactation. Therefore, the thrust of herd management strategies for reducing environmental exposure should focus on dry period and early lactation. During the dry period, susceptibility to intramammary infections is greatest at the 2 weeks after drying off and the 2 weeks prior to calving. Many infections acquired during the dry period persist to lactation and become clinical cases. Research has shown that 65% of coliform clinical cases that occur in the first 2 months of lactation are intramammary infections that originated during the dry period.22 Coliforms are adept at infecting the mammary gland during the transitional phase from lactating to fully involuted mammary gland. However, K pneumoniae, Serratia, and Pseudomonas are more capable than E coli at surviving in the mammary gland from the onset of involution until calving. Distribution of infections reveals that the greatest proportion of K pneumoniae infections present at calving originated in the first half of the dry period.24 E coli infections present at calving and early lactation most often originate during the last 2 weeks of the dry period. Rate of intramammary infections during lactation is highest at calving and decreases as days in milk advance. The prevalence coliform mastitis in a herd seldom exceeds 5% of lactating quarters because coliform infections tend to be short duration during lactation. The average duration of E coli intramammary infections during lactation is less than 10 days. Duration of intramammary infections caused by K pneumoniae average about 21 days. Chronic infections of greater than 90 days caused by E coli or K pneumoniae are relatively rare.22 A major difference between intramammary infections caused by coliform bacteria and those caused by other gram-negative bacteria is the duration that bacteria persist in the mammary gland. Intramammary infections caused by Serratia spp and Pseudomonas spp often are less severe and more likely chronic infections, compared with E coli intramammary infections, and may persist multiple lactations. The dynamics of environmental streptococcal mastitis across the stages of lactation are similar to those of coliform bacteria. The dry period is the time of greatest susceptibility to new environmental streptococcal intramammary infections. The rate of environmental streptococcal intramammary infections was 5.5-fold greater during the dry period than during lactation.24 Environmental streptococcal intramammary infections tended to be short-duration infections with only a relatively few becoming chronic. Average duration of environmental streptococcal intramammary infections is less than 2 weeks.22 During lactation, the incidence of clinical mastitis is greatest the first week after calving and decreased throughout the first 305 days in milk. Interestingly, rate of environmental streptococcal clinical cases increased in cows with extended lactations (⬎305 days) and is comparable to that of cows in peak lactation. Therefore, the use of management practices that encourage the use of extended calving intervals (thus a larger percentage of cows with extended days in milk) may impact the prevalence of environmental streptococcal intramammary infections in a herd. SUMMARY
Many of the practices and principals of management for reducing the exposure of dairy cows to environmental mastitis pathogens were introduced a quarter of a century ago22–25 and have been the subject of numerous reviews.1,3,21 The common theme for reducing mastitis pathogens in the cows’ environment is reducing moisture and organic contamination.1 Frequent manure removal, avoiding overstocking of cows, taking precautions to eliminate stagnant water around cows, and providing
Managing Environmental Mastitis
clean, dry inorganic bedding for cows to lay on are important management considerations. These factors of environmental hygiene transcend stall barns, manure pack barns, open corrals, and pasture systems. The emphasis of control should center on protecting periparturient animals during wet, hot periods of the year when mastitis pathogen growth in the environment is greatest. As the dairy industry in North America changes and progresses to adapt to economic, social, and environmental demands, the old adage of keeping cows cool, dry, and comfortable remains paramount in managing environmental mastitis. REFERENCES
1. Hogan J, Smith KL. Coliform mastitis. Vet Res 2003;34:507–19. 2. National Mastitis Council. Gram-negative bacteria. In: Laboratory handbook on bovine mastitis. Madison (WI): The National Mastitis Council, Inc; 1999. p. 85-115. 3. Hogan J, Smith KL. Environmental streptococcal mastitis: facts, fables, and fallacies. In: Proceedings of the 42nd Annual Meeting of the National Mastitis Council. Fort Worth (TX). Verona (WI): National Mastitis Council, Inc; 2003. p. 162–71. 4. Bramley AJ. Sources of Streptococcus uberis in the dairy herd. I. Isolation from bovine faeces and from straw bedding of cattle. J Dairy Res 1982;49:369 –73. 5. Kruze J, Bramley AJ. Sources of Streptococcus uberis in the dairy herd. II. Evidence of colonization of the bovine intestine by Str. uberis. J Dairy Res 1982;49:375–9. 6. Petersson-Wolfe CS, Adams S, Wolf SL, et al. Genomic typing of enterococci isolated from bovine mammary glands and environmental sources. J Dairy Sci 2008;91: 615–9. 7. Epperson WB, Hoblet KH, Smith KL, et al. Association of abnormal uterine discharge with new intramammary infection in the early postpartum period in multiparous dairy cows. J Am Vet Med Assoc 1993;202:1461– 4. 8. Rendos JJ, Eberhart RJ, Kesler EM. Microbial populations of teat ends of dairy cows, and bedding materials. J Dairy Sci 1975;58:1492–500. 9. Zdanowicz M, Shelford JA, Tucker CB, et al. Bacterial populations on teat ends of dairy cows housed in free stalls and bedded with either sand or sawdust. J Dairy Sci 2004;87;1694 –701. 10. Hogan JS, Smith KL, Hoblet KH, et al. Bacterial counts in bedding materials used on nine commercial dairies. J Dairy Sci 1989;72:250 – 8. 11. Kristula MA, Rogers W, Hogan JS, et al. Comparison of bacteria populations in clean and recycled sand used for bedding in dairy facilities. J Dairy Sci 2005;88:4317–25. 12. Gooch CA, Hogan JS, Glazier N, et al. Use of post-digested separated manure solids as freestall bedding: case study. In: Proceeding of the 46th Annual Meeting of the National Mastitis Council. Tampa (FL). Verona (WI): National Mastitis Council, Inc; 2006. p. 151– 60. 13. Hogan JH, Bogacz VL, Thompson LM, et al. Bacterial counts associated with sawdust and recycled manure bedding treated with commercial conditioners. J Dairy Sci 1999;82:1690 –5. 14. Hogan JS, Smith KL, Todhunter DA, et al. Bacterial counts associated with recycled newspaper bedding. J Dairy Sci 1990;73:1756 – 61. 15. Spencer H. Free stall and corral management as related to mastitis control. In: Proceedings of the Regional Meeting of the National Mastitis Council. Madison (WI). Verona (WI): National Mastitis Council, Inc; 1996. p. 60 –2. 16. Green MJ, Bradley AJ, Medley GF, et al. Cow, farm, and management factors during the dry period that determine the rate of clinical mastitis after calving. J Dairy Sci 2007;90:3764 –76.
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17. Lopez-Benavides MG, Williamson JH, Pullinger GD, et al. Field observations on the variation of Streptococcus uberis populations in a pasture-based dairy farm. J Dairy Sci 2007;90:5558 – 66. 18. Lacy-Hulbert J, Benavides ML, Williamson J, et al. Ecology of Streptococcus uberis within a pasture-based dairying system. Proceeding of the 46th Annual Meeting of the National Mastitis Council. Tampa (FL). Verona (WI): National Mastitis Council, Inc; 2006. p. 134 – 44. 19. Pankey JW. Hygiene at milking time in the prevention of bovine mastitis. Br Vet J 1989;145:401–9. 20. National Mastitis Council. Summary of peer-reviewed publications on efficacy of premilking and postmilking teat disinfectants published since 1980. In: Proceedings of the 51st Annual Meeting of the National Mastitis Council. St Petersburg (FL). Verona (WI): National Mastitis Council, Inc; 2012. p. 235– 49. 21. Smith KL, Hogan JS. Environmental mastitis. Large Anim Vet 1992;47:16 –20. 22. Smith KL, Todhunter DA, Schoenberger PS. Environmental mastitis: cause, prevalence, prevention. J Dairy Sci 1985;68:1531–53. 23. Hogan JS, Smith KL, Hoblet KH, et al. Field survey of mastitis in low somatic cell count herds. J Dairy Sci 1989;72:1547–56. 24. Smith KL, Todhunter DA, Schoenberger PS. Environmental pathogens and intramammary infection during the dry period. J Dairy Sci 1985;68:402–17. 25. Erskine RJ, Eberhart RJ, Hutchinson LH, et al. Incidence and types of clinical mastitis in dairy herds with high and low somatic cell counts. JAVMA 1988;192:761–5.
KEYWORDS • Mastitis • Bedding • Dairy cows • Intramammary infections KEY POINTS • Coliform bacteria, streptococci, and enterococci are the most common etiologic agents of environmental mastitis. • The primary agents of environmental mastitis are of fecal origin but can also heavily contaminate organic materials such as bedding, feed, and soil in the cows’ surroundings. • Washed sand contains 100-fold fewer mastitis pathogens per gram of bedding compared with common organic bedding materials. • Management keys to reducing exposure of cows to environmental mastitis pathogens include frequent manure removal, eliminating standing water in the cow’s walking lanes and loafing areas, and avoiding overcrowding of animals in barns and pastures. • Populations of mastitis pathogens increase in the cow’s environment as ambient temperature and moisture increases. • Rates of environmental mastitis are greatest during the dry period and early lactation compared with other stages of lactation.
The most common environmental mastitis pathogens among herds of North America are those grouped as coliforms and environmental streptococci. The term “coliform mastitis” frequently is used incorrectly to identify mammary disease caused by all gram-negative bacteria.1 Genera classified as coliforms are Escherichia, Klebsiella, and Enterobacter. Other gram-negative bacteria frequently isolated from intramammary infections include species of Serratia, Pseudomonas, and Proteus.2 Coliform bacteria occupy many habitats in the cow’s environment. Escherichia coli are normal inhabitants of the gastrointestinal tract of warm blooded animals. Both Klebsiella spp and Enterobacter spp populate soils, grains, water, and intestinal tracts of animals. Serratia marcesens share many environmental sources with Klebsiella spp and
Salaries and research support were provided by state and federal funds appropriated to the Ohio Agricultural Research and Development Center, The Ohio State University. The authors have nothing to disclose. Ohio Agricultural Research and Development Center, The Ohio State University, Wooster, OH 44691, USA * Corresponding author. E-mail address: [email protected] Vet Clin Food Anim 28 (2012) 217–224 http://dx.doi.org/10.1016/j.cvfa.2012.03.009 vetfood.theclinics.com 0749-0720/12/$ – see front matter © 2012 Elsevier Inc. All rights reserved.
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Enterobacter spp. Pseudomonas spp and Proteus spp commonly contaminate drop hoses used to wash udders before milking. The group of bacteria collectively labeled environmental streptococci includes Streptococcus uberis, Streptococcus dysgalcatiae, and Enterococcus spp.3 The environmental streptococci, S uberis in particular, have been isolated from bedding materials, soil, rumen, feces, vulva, lips, nares, mammary gland, and teats.4,5 Feed stuffs such as silages and green chop forages may also be a source of these pathogens and infections of the reproductive tract may contribute to environmental and teat end contamination.6 STALL BEDDING IS A KEY ENVIRONMENTAL SOURCE
The key to controlling environmental mastitis to an economically acceptable level within a herd is to reduce the exposure of cows to the pathogens. Although bacteria that cause environmental mastitis are among the etiologic agents commonly responsible for infectious respiratory and urogenital diseases in dairy cows,7 the spread of these bacteria from other regions of the body to the mammary gland via the vascular or lymphatic systems appears minimal. Intramammary infections caused by environmental mastitis pathogens typically result from the bacteria traversing the teat canal and multiplying in the gland. These bacterial species are chemotropic organisms requiring organic material to use as food. Coliforms and streptococci cannot live on teat skin for long periods of time. If these bacteria are present in large numbers on teat skin, it is the result of recent contamination. Therefore, the number of these bacteria on teat skin is a reflection of the cow’s exposure to the contaminating environment.8,9 Cows lay down 12 to 14 hours a day, and their teats are in direct contact with the bedding or other materials where they rest. Populations of the bacteria in bedding are related to the number of bacteria on teat ends and rates of clinical mastitis.9,10 Therefore, reducing the number of bacteria in bedding generally results in a decrease in environmental mastitis. Coliforms cannot live on teat skin for long periods of time. If these bacteria are present in large numbers on teat skin, it is the result of recent contamination from a source such as bedding. Hygiene and proper management of stall, lots, and pastures are essential. Sand Bedding
Ideally, bedding should be inorganic materials that are low in moisture content and contain few nutrients for bacteria to use. The bedding material that we recommend most for controlling environmental mastitis is washed sand. Compared to organic materials such as sawdust, recycled manure, straw, and dirt, washed sand consistently contains 100-fold fewer mastitis pathogens per gram of bedding.10 The effectiveness of sand for reducing exposure of mastitis pathogens to mammary glands is due to the inorganic properties of sand. However, as organic content and moisture in sand bedding increase during the common practice of on-farm reclaiming sand from sand-laden manure, the mastitis pathogen populations also increase.11 A realistic goal for dry matter of sand used for bedding is greater than 95%. Organic matter in sand bedding should be less than 5%. Organic Bedding
Many farms are forced to use organic bedding materials that are compatible with liquid manure– handling systems. Little advantage exists in using one organic material over the use of another. For example, straw tends to have highest streptococcal counts, while sawdust has the highest coliform counts in comparisons among these
Managing Environmental Mastitis
bedding materials.10 Any material to be used as bedding should be stored in a dry area to prevent saturation by rain and ground moisture. Composting organic materials is an effective way to reduce bacterial counts before use as bedding. However, although many organic bedding materials have relatively few mastitis pathogens prior to use, the pathogen populations often increase 10,000-fold within hours after use as bedding.12 Fresh bedding tends to absorb moisture from the cows’ environment for use by the great number of bacteria that are constantly present in manure and soiled bedding. Organic materials used as bedding in North America have historically been affordable byproducts of the grain crops or the forestry and wood industry. Two trends have caused a shift from these organic bedding sources to the use of recycled manure solids on many dairies. First, the availability of sawdust, wood shavings, and straw has diminished with the increased of use of these products for home heating fuel and landscaping mulch. Second, the use of methane digesters on some dairies results in available solids and the profitability of digesters necessitates the use of solids for bedding. In general, bacterial counts in manure solids are similar to those in sawdust. The key to successful use of manure solids is to lower the moisture content, thus lowering the bacterial counts of mastitis pathogens. A realistic goal for manure solids when placed in stalls is 35% dry matter. Regardless of the bedding used, removing wet and soiled material from the back third of stalls will significantly reduce the bacterial counts. Stalls should be raked a minimum of twice daily when animals are moved to be milked. A practice that is often successful in herds using manure solids is the daily complete replacement of bedding in back third of stalls. Spraying bedding with disinfectant and adding powdered lime to bedding have met with little practical success in reducing bacterial counts.13 These practices cause an initial decline in bacterial populations, but pathogen numbers quickly recover. Twice-a-day application of powdered lime may be necessary to sustain an advantage in lowering bacterial numbers. Standing water and mud should be avoided in stalls, holding areas, and lots. Overcrowding of free-stall barns increases the manure contaminating the alleys and lanes. The accumulated manure in alleys will splatter on hooves and legs to contaminate bedding with organic matter and inoculate the bedding with fecal bacteria. Cows’ access to dirt-manure lots also should be limited during rainy seasons. Outbreaks of coliform mastitis are common during rainy seasons when cows are exposed to dirt-manure lots and lanes leading to the milking parlors. Seasonal Effects
Climatic factors that affect the risk to environmental mastitis are temperature and humidity. As the ambient temperature and moisture increase, populations of pathogens increase in the cow’s environment and the mammary defense systems to combat infections become compromised. Growth rates of coliforms and environmental streptococci are greatest during warm, wet weather. The effects of season on bacterial populations in bedding are quite dramatic in regions that experience a wide variation of temperatures within a year. In general, the impact of bedding on exposure of cows in confinement housing decreases during cold weather and increases as temperatures and humidity increase.10 Previous trials have shown a strong correlation between bacterial counts in bedding and both ambient temperature and relative humidity.14 Overcrowding of barns with cows will exasperate the effects of heat and humidity. Therefore, adequate ventilation of barns and proper stocking rates are essential to moderate the effects of heat and humidity in housing areas.
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Dry Lots and Corrals
Dirt and manure covered corrals are commonly used to house cows in semiarid and arid areas where temperatures are seldom below freezing for an extended time. Exposure to pathogens generally is low during the dry seasons as moisture content of the dirt-manure mixture is low. However, as density of cows increase under shade structures and around feeding areas and water troughs, excess wet organic matter should be removed or spread out to be dried.15 Climatic factors affecting exposure in herds where cows are maintained on dry lots differ from those of in-stall barns. The rainy seasons of late fall through early spring are when bacterial populations are greatest. Manure in dry lots during the summer tends to be desiccated, thus limiting the moisture essential for bacterial growth. Grazing Systems
The majority of research on the effects of grazing systems on mammary health has been conducted outside of North America. However, the overriding principle of reducing pathogen exposure by the use of grazing pastures appears universal. Grazing management systems often decrease pathogen loads in the cows’ environment compared with total confinement systems. Turf-covered soil in grazing paddocks typically have minimal contamination with environmental mastitis pathogens when compared with organic bedding in stalls or loose housing. Bacterial exposure increases as forage is closely grazed and stocking rate increases.16,17 Ample time between rotation of cows on paddocks is needed to allow forage regrowth over soil and manure load to dissipate. Barren soil due to overgrazing and trampling can harbor elevated populations in the cows’ environment.18 Areas around feed troughs, exercise lots, and lanes often expose cows to bacterial concentrations comparable to that in organic bedded stalls. Removal of wet organic matter and replacement with dry, inorganic materials will reduce exposure. Similar to dry lots, solar radiation and drying during summer months reduce bacterial contamination in these areas compared with rainy winter months.17 Maternity and Dry Cow Lots
As evidenced later in the article, the rate of new intramammary infections caused by environmental mastitis pathogens is greater during the dry period than during lactation. Management and hygiene of dry cow housing and maternity areas should be priorities. Fortunately, the management practices for reducing mastitis pathogen exposure in dry cow and maternity facilities are similar to those for lactating cow housing. Dry cow areas should be well drained and free of excess manure. Dirt-covered areas can expose cows to pathogen levels comparable to those in free-stalls. Box stalls and loose housing areas should be cleaned to the foundation base regularly. Manure packs are to be avoided because they generally contain extremely high counts of pathogens that are dangerous to both dam and calf. Milking Hygiene
Milking time hygiene is the basis for control of contagious mastitis but has less influence on environmental mastitis. The use of germicidal teat dips postmilking will have minimal effect on incidence of new intramammary infections caused by coliform or environmental streptococci. Teat dip efficacy is dependent on the time of application relative to milking and the pathogens causing mastitis. Most germicidal teat dips effectively and rapidly destroy microbes on teat skin by chemical or biological action. However, the persistency of germicidal activity is limited and
Managing Environmental Mastitis
neutralized by organic material such as milk and manure.1 Therefore, although most germicidal products will kill coliforms on teat skin, exposure to these pathogens occurs primarily between milkings, long after the killing activity of the dips has diminished. Predipping teats before milking in an effective disinfectant reduces new intramammary infections caused by coliforms during lactation. Field trials have shown predipping reduces the incidence of clinical mastitis by 50% in herds with low levels of contagious mastitis.19 Current recommendations in North America for predipping include forestripping the first few streams of milk, removing excess manure and dirt from teats, dipping teats in the germicidal teat dip, allowing teat dip to contact teat skin at least 30 seconds, and manually drying teats with either individual paper towels or freshly laundered cloth towels. Barrier dips form a physical obstruction between teat skin and the environment. Latex, acrylic, and polymer based products form a physical seal over the teat end to impede entrance into the udder between milkings. The use of some latex barrier teat dips may reduce the incidence of coliform mastitis, but the efficacy of physical barrier teat dips against other pathogens is minimal. Barrier teat dips containing germicides have not been shown to be more effective than conventional germicidal dips in reducing environmental mastitis in controlled studies.20 MONITORING CLINICAL MASTITIS
The ultimate measure of success in reducing exposure to environmental mastitis pathogens is improvement in mammary health. Bulk tank and monthly cow somatic cell counts (SCCs) are poor milk quality indicators of environmental mastitis. The prevalence of intramammary infections caused by environmental pathogens within a herd is seldom great enough to cause bulk tank SCCs of higher than 250,000/mL, but approximately 85% of coliform and 50% of environmental streptococcal infections will cause clinical mastitis. Surveys of herds with low bulk tank SCCs21 have shown the average rate of clinical mastitis to be 46 cases per year in a 100-cow herd (3.8% of cows per month). The high frequency of clinical cases and relatively short duration of these intramammary infections render the use of individual cow SCC and bulk tank SCC as poor indicators of the prevalence of disease caused by these bacteria. For example, prevalence of intramammary infections caused by environmental mastitis pathogens seldom exceeds 5% of quarters in a herd; however, 20% and 15% of cows in well-managed herds are annually diagnosed with clinical mastitis caused by coliforms and environmental streptococci, respectfully. A realistic goal for rate of total clinical cases in a well-managed herd is 2% of cows per month. The severity of clinical mastitis caused by environmental pathogens ranges from mild local signs to death. The vast majority of clinical coliform and environmental streptococcal clinical cases are characterized by only abnormal milk and a swollen gland. Only about 10% of clinical coliform cases result in systemic signs including fever, anorexia, and altered respiration.22,23 Despite the relatively low percentage of clinical coliform cases yielding systemic signs, coliform bacteria have an exaggerated reputation for causing severe mastitis. The basis for this distinction originates from the point that the coliforms are the most common cause of systemic illness resulting from mastitis. Survey averages suggest that coliform bacteria are the culprits of 60% to 70% of severe clinical cases involving systemic signs.22,23 Therefore, the general conclusions concerning severity of clinical coliform cases are that few coliform intramammary infections cause systemic clinical signs, but the majority of clinical cases resulting in systemic signs are caused by coliform bacteria. Stage of lactation has a tremendous impact on cows’ susceptibility to environmental mastitis. Recording the number of clinical cases and documenting the stage of
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lactation when they occur will aid in determining when cows are at greatest risk to clinical mastitis. Rates of new intramammary infections caused by coliforms are generally greater during the dry period than during lactation. Therefore, the thrust of herd management strategies for reducing environmental exposure should focus on dry period and early lactation. During the dry period, susceptibility to intramammary infections is greatest at the 2 weeks after drying off and the 2 weeks prior to calving. Many infections acquired during the dry period persist to lactation and become clinical cases. Research has shown that 65% of coliform clinical cases that occur in the first 2 months of lactation are intramammary infections that originated during the dry period.22 Coliforms are adept at infecting the mammary gland during the transitional phase from lactating to fully involuted mammary gland. However, K pneumoniae, Serratia, and Pseudomonas are more capable than E coli at surviving in the mammary gland from the onset of involution until calving. Distribution of infections reveals that the greatest proportion of K pneumoniae infections present at calving originated in the first half of the dry period.24 E coli infections present at calving and early lactation most often originate during the last 2 weeks of the dry period. Rate of intramammary infections during lactation is highest at calving and decreases as days in milk advance. The prevalence coliform mastitis in a herd seldom exceeds 5% of lactating quarters because coliform infections tend to be short duration during lactation. The average duration of E coli intramammary infections during lactation is less than 10 days. Duration of intramammary infections caused by K pneumoniae average about 21 days. Chronic infections of greater than 90 days caused by E coli or K pneumoniae are relatively rare.22 A major difference between intramammary infections caused by coliform bacteria and those caused by other gram-negative bacteria is the duration that bacteria persist in the mammary gland. Intramammary infections caused by Serratia spp and Pseudomonas spp often are less severe and more likely chronic infections, compared with E coli intramammary infections, and may persist multiple lactations. The dynamics of environmental streptococcal mastitis across the stages of lactation are similar to those of coliform bacteria. The dry period is the time of greatest susceptibility to new environmental streptococcal intramammary infections. The rate of environmental streptococcal intramammary infections was 5.5-fold greater during the dry period than during lactation.24 Environmental streptococcal intramammary infections tended to be short-duration infections with only a relatively few becoming chronic. Average duration of environmental streptococcal intramammary infections is less than 2 weeks.22 During lactation, the incidence of clinical mastitis is greatest the first week after calving and decreased throughout the first 305 days in milk. Interestingly, rate of environmental streptococcal clinical cases increased in cows with extended lactations (⬎305 days) and is comparable to that of cows in peak lactation. Therefore, the use of management practices that encourage the use of extended calving intervals (thus a larger percentage of cows with extended days in milk) may impact the prevalence of environmental streptococcal intramammary infections in a herd. SUMMARY
Many of the practices and principals of management for reducing the exposure of dairy cows to environmental mastitis pathogens were introduced a quarter of a century ago22–25 and have been the subject of numerous reviews.1,3,21 The common theme for reducing mastitis pathogens in the cows’ environment is reducing moisture and organic contamination.1 Frequent manure removal, avoiding overstocking of cows, taking precautions to eliminate stagnant water around cows, and providing
Managing Environmental Mastitis
clean, dry inorganic bedding for cows to lay on are important management considerations. These factors of environmental hygiene transcend stall barns, manure pack barns, open corrals, and pasture systems. The emphasis of control should center on protecting periparturient animals during wet, hot periods of the year when mastitis pathogen growth in the environment is greatest. As the dairy industry in North America changes and progresses to adapt to economic, social, and environmental demands, the old adage of keeping cows cool, dry, and comfortable remains paramount in managing environmental mastitis. REFERENCES
1. Hogan J, Smith KL. Coliform mastitis. Vet Res 2003;34:507–19. 2. National Mastitis Council. Gram-negative bacteria. In: Laboratory handbook on bovine mastitis. Madison (WI): The National Mastitis Council, Inc; 1999. p. 85-115. 3. Hogan J, Smith KL. Environmental streptococcal mastitis: facts, fables, and fallacies. In: Proceedings of the 42nd Annual Meeting of the National Mastitis Council. Fort Worth (TX). Verona (WI): National Mastitis Council, Inc; 2003. p. 162–71. 4. Bramley AJ. Sources of Streptococcus uberis in the dairy herd. I. Isolation from bovine faeces and from straw bedding of cattle. J Dairy Res 1982;49:369 –73. 5. Kruze J, Bramley AJ. Sources of Streptococcus uberis in the dairy herd. II. Evidence of colonization of the bovine intestine by Str. uberis. J Dairy Res 1982;49:375–9. 6. Petersson-Wolfe CS, Adams S, Wolf SL, et al. Genomic typing of enterococci isolated from bovine mammary glands and environmental sources. J Dairy Sci 2008;91: 615–9. 7. Epperson WB, Hoblet KH, Smith KL, et al. Association of abnormal uterine discharge with new intramammary infection in the early postpartum period in multiparous dairy cows. J Am Vet Med Assoc 1993;202:1461– 4. 8. Rendos JJ, Eberhart RJ, Kesler EM. Microbial populations of teat ends of dairy cows, and bedding materials. J Dairy Sci 1975;58:1492–500. 9. Zdanowicz M, Shelford JA, Tucker CB, et al. Bacterial populations on teat ends of dairy cows housed in free stalls and bedded with either sand or sawdust. J Dairy Sci 2004;87;1694 –701. 10. Hogan JS, Smith KL, Hoblet KH, et al. Bacterial counts in bedding materials used on nine commercial dairies. J Dairy Sci 1989;72:250 – 8. 11. Kristula MA, Rogers W, Hogan JS, et al. Comparison of bacteria populations in clean and recycled sand used for bedding in dairy facilities. J Dairy Sci 2005;88:4317–25. 12. Gooch CA, Hogan JS, Glazier N, et al. Use of post-digested separated manure solids as freestall bedding: case study. In: Proceeding of the 46th Annual Meeting of the National Mastitis Council. Tampa (FL). Verona (WI): National Mastitis Council, Inc; 2006. p. 151– 60. 13. Hogan JH, Bogacz VL, Thompson LM, et al. Bacterial counts associated with sawdust and recycled manure bedding treated with commercial conditioners. J Dairy Sci 1999;82:1690 –5. 14. Hogan JS, Smith KL, Todhunter DA, et al. Bacterial counts associated with recycled newspaper bedding. J Dairy Sci 1990;73:1756 – 61. 15. Spencer H. Free stall and corral management as related to mastitis control. In: Proceedings of the Regional Meeting of the National Mastitis Council. Madison (WI). Verona (WI): National Mastitis Council, Inc; 1996. p. 60 –2. 16. Green MJ, Bradley AJ, Medley GF, et al. Cow, farm, and management factors during the dry period that determine the rate of clinical mastitis after calving. J Dairy Sci 2007;90:3764 –76.
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17. Lopez-Benavides MG, Williamson JH, Pullinger GD, et al. Field observations on the variation of Streptococcus uberis populations in a pasture-based dairy farm. J Dairy Sci 2007;90:5558 – 66. 18. Lacy-Hulbert J, Benavides ML, Williamson J, et al. Ecology of Streptococcus uberis within a pasture-based dairying system. Proceeding of the 46th Annual Meeting of the National Mastitis Council. Tampa (FL). Verona (WI): National Mastitis Council, Inc; 2006. p. 134 – 44. 19. Pankey JW. Hygiene at milking time in the prevention of bovine mastitis. Br Vet J 1989;145:401–9. 20. National Mastitis Council. Summary of peer-reviewed publications on efficacy of premilking and postmilking teat disinfectants published since 1980. In: Proceedings of the 51st Annual Meeting of the National Mastitis Council. St Petersburg (FL). Verona (WI): National Mastitis Council, Inc; 2012. p. 235– 49. 21. Smith KL, Hogan JS. Environmental mastitis. Large Anim Vet 1992;47:16 –20. 22. Smith KL, Todhunter DA, Schoenberger PS. Environmental mastitis: cause, prevalence, prevention. J Dairy Sci 1985;68:1531–53. 23. Hogan JS, Smith KL, Hoblet KH, et al. Field survey of mastitis in low somatic cell count herds. J Dairy Sci 1989;72:1547–56. 24. Smith KL, Todhunter DA, Schoenberger PS. Environmental pathogens and intramammary infection during the dry period. J Dairy Sci 1985;68:402–17. 25. Erskine RJ, Eberhart RJ, Hutchinson LH, et al. Incidence and types of clinical mastitis in dairy herds with high and low somatic cell counts. JAVMA 1988;192:761–5.