Best Management Practices to Reduce Mastitis and Improve Milk Quality


Production of maximum quantities of high-quality milk is an important goal of every dairy operation. Poor milk quality affects all segments of the dairy industry, ultimately resulting in milk with decreased manufacturing properties and dairy products with reduced shelf life. Mastitis can be a significant contributor to reduced milk quality. This disease is an inflammation of the udder that affects a high proportion of dairy cows throughout the world. Mastitis differs from most other animal diseases in that several diverse bacteria are capable of infecting the udder. These pathogens invade the udder, multiply there, and produce harmful substances that result in inflammation, reduced milk production, and altered milk quality. Because mastitis can be caused by many different pathogens, control is extremely difficult, and economic losses due to mastitis can be immense. The NMC estimates that mastitis costs dairy producers in the U.S. over $2 billion annually. Thus, mastitis continues to be one of, if not, the most significant limiting factor to profitable dairy production in the U.S. and throughout the world.

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Why Should We Be Concerned about Milk Quality?

The quality of milk has been and continues to be a topic of intense debate. One important measure of milk quality is the number of somatic cells in milk, referred to as the somatic cell count (SCC). Milk with a high SCC is produced by cows with mastitis and is of inferior quality. In the U.S., the current regulatory limit for somatic cells defined in the 2007 Grade A Pasteurized Milk Ordinance (PMO) is 750,000/ml of milk. Recently, California lowered its state SCC regulatory standard for legal milk to 600,000 cells/ml. There is continuing pressure from a variety of advocacy groups to reduce the regulatory limit for somatic cells in milk from the current 750,000/ml to 400,000 or less to be competitive in the global dairy marketplace. Global standards are considerably lower (400,000 somatic cells/ml) and as low as 150,000 to 200,000/ml in some of the Scandinavian countries. Thus, this disparity in SCC makes it difficult, if not impossible, to export U.S.-produced milk and milk products to other developed countries.

A recent report was published by the USDA Animal Improvement Program Laboratory (see Miller et al., 2008) on SCC data from all herds in the U.S. enrolled in the Dairy Herd Improvement (DHI) testing program for 2007 (Table 1). The good news is that the national SCC average for 2007 was 276,000 cells/ml of milk, which is 12,000 cells/ml lower than in 2006. The bad news was that 3.5% of herds in the U.S. had >750,000 SCC/ml, and 24% of the national dairy herd had >400,000 SCC/ml. Variation among states was large. State average SCCs were often lower than the national average in the Northeast, Upper Midwest, and the far West and higher in the Southeast, Mid-Atlantic, and Central states — a finding consistent with previous reports. The Southern Region had the poorest quality milk of all regions of the U.S., an average of 37% higher than the national average. In 2007, six states had average SCCs of >400,000/ml, and all were in the Southern Region (Table 1).

Table 1. Characteristics of DHI herd test days for milk yield and SCC by state during 2007.
State Herd test days1 Cows2 per herd Avg daily milk yield Average SCC % Herd test days3 with SCC greater than:
(No.) (No.) (Pounds) (Cells/ml X 1000) 750,000 cells/ml 600,000 cells/ml 500,000 cells/ml 400,000 cells/ml
Alabama 238 122.3 50.6 407 4.2 10.1 22.7 42.9
Arizona 264 1451.6 69.6 257 0.0 0.8 1.9 7.6
Arkansas 329 108.4 55.1 441 15.8 24.9 35.6 53.5
California 9,327 702.0 73.9 253 2.4 4.8 7.7 13.7
Colorado 343 689.0 69.3 268 1.2 3.5 7.9 14.3
Connecticut 807 92.6 67.5 285 3.6 6.7 11.5 20.0
Delaware 251 116.2 68.3 320 2.4 4.4 8.8 20.3
Florida 222 755.6 69.0 333 8.6 18.5 27.0 50.9
Georgia 1,134 134.7 61.2 422 6.7 17.8 31.7 51.8
Idaho 1,718 684.9 75.5 255 1.7 3.8 8.1 14.7
Illinois 4,427 86.0 69.5 294 3.0 7.4 13.9 26.7
Indiana 3,621 84.8 69.1 306 4.6 9.6 15.6 28.6
Iowa 8,918 91.9 71.0 304 4.2 9.6 16.3 29.3
Kansas 2,021 95.7 66.6 360 6.8 14.4 22.8 37.9
Kentucky 1,721 79.8 63.3 354 6.0 14.3 23.8 39.7
Louisiana 448 106.2 51.2 446 13.6 29.0 42.4 60.7
Maine 1,208 72.3 63.7 267 3.1 6.5 12.7 21.5
Maryland 3,616 80.3 66.3 284 3.3 7.4 12.3 22.2
Massachusetts 831 79.2 68.2 276 2.0 5.2 9.7 17.9
Michigan 7,678 151.4 78.1 247 2.3 4.8 8.6 16.5
Minnesota 25,131 78.6 69.9 320 4.7 10.3 18.1 31.3
Mississippi 336 162.6 64.9 337 2.4 10.4 18.2 41.1
Missouri 3,399 65.5 58.3 356 6.9 13.7 21.8 36.5
Montana 400 115.9 75.2 200 0.0 0.5 2.0 6.3
Nebraska 1,591 127.0 68.1 331 6.2 12.5 21.5 36.0
Nevada 116 540.5 78.3 306 7.8 7.8 11.2 12.9
New Hampshire 873 84.5 69.9 245 1.8 4.2 8.4 17.1
New Jersey 565 63.8 65.8 344 4.4 10.3 18.6 33.3
New Mexico 255 1391.4 70.8 289 5.5 7.1 12.9 19.2
New York 20,265 112.4 71.2 258 2.4 5.8 11.0 20.5
North Carolina 1,644 125.8 68.2 324 2.0 6.1 12.9 26.9
North Dakota 384 88.2 69.3 320 2.1 4.2 10.7 22.4
Ohio 8,534 89.1 68.8 317 3.6 8.1 14.9 26.7
Oklahoma 582 123.6 57.9 343 6.7 15.1 27.5 44.3
Oregon 2,255 154.4 67.6 228 2.8 4.6 7.6 12.0
Pennsylvania 42,727 59.4 69.4 296 3.0 7.2 13.2 24.1
Puerto Rico 956 110.5 36.1 499 18.5 30.3 45.5 63.4
Rhode Island 41 73.0 62.6 160 0.0 0.0 0.0 9.8
South Carolina 538 161.2 62.8 355 2.0 5.2 12.3 33.1
South Dakota 1,372 154.3 71.2 288 5.4 12.7 22.2 36.2
Tennessee 1,525 86.7 59.6 418 5.2 14.8 27.6 49.6
Texas 1,563 396.4 61.5 318 2.8 6.5 12.5 26.2
Utah 1,397 163.8 69.0 242 2.6 4.8 8.3 16.7
Vermont 3,478 101.0 67.6 230 1.5 3.5 6.7 13.6
Virginia 4,034 107.3 68.5 309 2.0 5.6 10.9 23.8
Washington 1,842 240.5 74.4 237 2.0 2.9 4.6 8.7
West Virginia 409 84.8 60.1 324 3.7 8.3 18.8 33.0
Wisconsin 52,264 80.9 74.5 258 3.3 6.7 11.2 19.8
Wyoming 28 162.5 70.9 320 0.0 0.0 0.0 7.1
U.S. 227,626 125.1 71.4 276 3.5 7.6 13.4 24.0
1All herd test days with usable records. This includes records missing sire identification but having acceptable information in other fields.
2 Cows with usable records (less than total cows on test).
3Herd test days with 10 or more usable records.


The SCC of milk produced by dairy farms in the Southern Region over the last 10 years is presented in Table 2. The average SCC during this period was about 35% higher in the Southern Region than the U.S. average, with a yearly range of approximately 30% higher in 2000 to almost 41% higher than the U.S. average in 2003. Texas and Virginia consistently had the lowest annual average SCC, and Oklahoma, North Carolina, Kentucky, and South Carolina had average SCCs <400,000. On the other hand, Florida, Louisiana, Tennessee, Alabama, Puerto Rico, Arkansas, Mississippi, and Georgia had the highest average annual SCC from 1998–2007 that were generally >400,000/ml and sometimes in excess of 500,000/ml. Data in Table 2 also demonstrate that dairy producers in many states in the Southern Region are making progress toward lowering SCCs. For example, the average SCC decreased substantially in Tennessee over the last two years from 504,000/ml in 2005 to 418,000/ml in 2007. This coincides with the launch of the Tennessee Quality Milk Initiative, a science-based comprehensive program to enhance milk quality and thus improve the profitability and sustainability of dairy farms in Tennessee via an educational, research, and outreach approach. However, data in Table 2 also demonstrate quite clearly that there is much room for continued improvement as a high proportion of herds in the Southeast still have cell counts in the 400,000 to 600,000 range.


Table 2. DHI SCC in Southern Region from 1998-2007. Data is in thousands of cells per milliliter of milk.
State 1998 1999 2000 2001 2002 2003 2004 2005 2006 2007 Average
Alabama 420 427 441 444 485 517 455 433 432 407 446
Arkansas 410 448 427 486 436 387 404 448 457 441 434
Florida 508 533 504 548 529 633 475 473 319 333 486
Georgia 429 411 409 407 432 479 418 433 428 422 427
Kentucky 405 376 370 413 412 419 383 392 395 354 392
Louisiana 455 454 476 479 525 498 449 416 456 446 465
Mississippi 450 456 448 442 498 480 425 386 368 337 429
North Carolina 377 366 370 364 371 414 365 358 355 324 366
Oklahoma 392 387 396 483 403 356 357 363 333 343 381
Puerto Rico 408 423 475 412 471 441 459 429 443 499 446
South Carolina 423 389 379 404 389 448 390 387 383 355 395
Tennessee 501 446 420 413 463 476 469 504 463 418 457
Texas 297 288 294 342 316 364 308 346 282 318 316
Virginia 355 329 338 333 330 374 336 320 331 309 336
Southeast Average 416 410 411 426 433 449 407 406 389 379 413
U.S. Average 318 311 316 322 313 319 295 296 288 276 305
% Difference 30.8 31.7 29.9 32.3 38.3 40.8 38.0 37.3 35.0 37.3 35.4


Another important milk quality issue relates to human health. Opponents claim that there is no human health risk associated with high bulk tank SCC milk; therefore, the SCC limit in the PMO should not be lowered. However, milk with a high SCC is associated with a higher incidence of antibiotic residues in milk and the presence of pathogenic organisms and toxins in milk. Last, but certainly not least, is the fact that poor-quality milk is an inferior product with reduced processing properties, resulting in dairy products with a reduced shelf life. Thus, milk with a high SCC is associated with indirect health risks to the consumer and is an inferior-quality product. Good-quality milk lasts longer, tastes better, and is more nutritious. These issues are the basis for animal health advocacy groups to lower the SCC regulatory limit.

A mandated reduction in the number of somatic cells in milk via regulatory intervention may not be necessary because in the near future milk buyers may only purchase milk of excellent quality. Recently, some dairy processing plants have made changes to their milk quality requirements for incoming raw milk. These changes have occurred, in part, by demands from retailers and major food service companies for milk with a higher quality with a longer shelf life. Eventually, changes in SCC limits and perhaps even requirements for raw milk to be free of specific bacteria could be implemented. Thus, SCC limits for raw milk to be acceptable at dairy processing plants may decrease to levels much lower than they are now, making it increasingly problematic for dairy producers to meet these higher standards. Production of better-quality milk will place a much greater emphasis on strategies for the prevention and control of mastitis to reduce the number of somatic cells in milk.

What Is Mastitis?

Mastitis, an inflammation of the mammary gland caused by bacterial infection, trauma, or injury to the udder, remains the most common and most expensive disease affecting dairy cattle throughout the world. Mastitis is caused by several different bacteria that can invade the udder, multiply there, and produce harmful substances that result in inflammation. Mastitis reduces milk yield and alters milk composition. The magnitude of reduced milk yield and alterations in milk composition is influenced by the severity of the inflammatory response, which in turn is influenced by the mastitis pathogen causing the infection. Clinical mastitis is characterized by abnormal milk and/or visible abnormalities of the udder such as hot and swollen quarters. However, subclinical mastitis (often referred to as hidden mastitis), the most common form of mastitis, is not readily apparent because there are no visible signs of the disease.

Cows with clinical mastitis have more dramatic changes in milk yield and composition than cows with subclinical mastitis. Results of studies published thus far support the contention that alterations in milk composition associated with mastitis are due to several factors including impaired milk synthesis and secretion, mammary epithelial cell death and degeneration, and transport of substances from blood to milk and from milk to blood. The most notable changes in milk composition associated with mastitis are decreased concentrations of fat, lactose, casein, and calcium; and increased concentrations of albumin, sodium, and chloride. Concentrations of lipases, proteases, oxidases, plasmin, and plasminogen increase, which may adversely influence milk stability, milk flavor, and processed dairy products. In addition, factors not normally found in milk such as inflammatory mediators and bacterial enterotoxins and endotoxins have been detected in milk from cows with mastitis. From a dairy manufacturing perspective, mastitis decreases concentrations of desirable components and increases concentrations of undesirable components, all of which influence the shelf life and taste of milk.

The measurement used most commonly to detect subclinical mastitis is the SCC of milk. One characteristic feature of mammary gland inflammation is an elevation in the number of somatic cells in milk. Milk from uninfected mammary glands contains <100,000/ml. A milk SCC >200,000/ml suggests that an inflammatory response has been elicited, that a mammary quarter is infected or is recovering from an infection, and is a clear indication that milk has reduced manufacturing properties. Thus, an increase in the SCC of milk is a good indicator of inflammation in the udder. Infection of the udder by mastitis pathogens alters milk composition and reduces milk yield. Most studies that evaluated the influence of mastitis on the composition of milk used SCC as the basis for determining the infection status of udders and for determining the degree of inflammation.

The bulk tank SCC (BTSCC) has been used to gauge the udder infection status of a dairy herd and also gives a good indication of the loss in milk production in a herd due to mastitis. As the BTSCC increases, the percentage of mammary quarters infected increases, and the percentage production loss increases. Similarly, as the percentage of cows with a SCC >800,000 increases, rolling herd production decreases. Small increases in SCC can impact production. Most herd milk contains between 200,000 to 500,000 somatic cells/ml of milk. These herds are losing at least 8% in potential milk production. Thus, methods of mastitis control that reduce SCC will improve milk yield and composition and decrease economic losses due to mastitis.

Controlling Mastitis

Prevention and Control of Mastitis: Mastitis is a difficult disease to control because many different bacteria are capable of infecting the udder and producing the disease. Microorganisms that most frequently cause mastitis can be divided into two broad categories: (1) contagious pathogens, which are spread from cow to cow primarily during the milking process; and (2) environmental pathogens, which are found throughout the habitat of dairy cows.

Contagious Mastitis Pathogens: Contagious mastitis is caused primarily by Staphylococcus aureus and Streptococcus agalactiae. Mycoplasma bovis and other Mycoplasma species have been increasingly reported as important contagious mastitis pathogens. The primary source of these organisms is the udder of infected cows. Contagious mastitis pathogens spread from infected cows to uninfected cows primarily at milking. Some characteristics of herds with a contagious mastitis problem include: (1) a high prevalence of intramammary infection (IMI) during lactation, (2) a high BTSCC, (3) infections of long duration, (4) low proportion of infections resulting in clinical mastitis (infections mostly subclinical), and (5) a low prevalence of infection during the dry period.

Environmental Mastitis Pathogens: Environmental mastitis is caused primarily by environmental streptococci including Streptococcus uberis, Streptococcus dysgalactiae subsp. dysgalactiae, and coliforms including Escherichia coli and Klebsiella species. The primary source of environmental mastitis pathogens is the environment of the cow. Infections generally occur between milkings and during the milking process. Some characteristics of herds with an environmental mastitis problem include: (1) a low prevalence of IMI during lactation, (2) a low BTSCC, (3) infections of short duration, (4) many IMI resulting in clinical mastitis, and (5) a high prevalence of infection during the dry period.

Mastitis Control Strategies: Current mastitis control programs are based on hygiene and include teat disinfection, antibiotic therapy, and culling of chronically infected cows. Acceptance and application of these measures throughout the world has led to considerable progress in controlling mastitis caused by contagious mastitis pathogens such as Strep. agalactiae and Staph. aureus. However, as the prevalence of contagious mastitis pathogens was reduced, the proportion of IMI caused by environmental pathogens such as E. coli and Strep. uberis has increased markedly. Therefore, it is not surprising that mastitis caused by coliforms and environmental Streptococcus species has become a major problem in many well-managed dairy farms that have successfully controlled contagious pathogens.

Controlling mastitis is not simply a matter of doing just one thing. Rather, the control of mastitis involves a number of steps that constitute a control program. Mastitis control programs should have the following characteristics: (1) practical, (2) economical, (3) subject to easy modification, and (4) effective under most management conditions. Two different approaches are outlined regarding mastitis management. The first approach is aimed at herds that have a serious problem and where immediate action is necessary. The second more comprehensive approach is the preferred strategy that should be applicable to the majority of dairy herds (see Philpot and Nickerson, 1991).

Herds with a high SCC will likely need to adopt a short-term goal of reducing SCC as quickly as possible so that milk can meet standards as set forth in the PMO. This will require extensive use of highly trained personnel and laboratory facilities and consequently is an expensive approach. Some goals would be to confirm the extent of infection, identify the bacteria causing mastitis, and identify cows to be treated or culled from the herd. One excellent method of making some of these important decisions is through a SCC program. This is relatively inexpensive, and SCC data can be used by dairy producers, veterinarians, extension personnel, and dairy consultants for making educated decisions regarding: (1) cows to be sampled for microbiological culture, (2) cows to be culled, (3) milking order of cows, and (4) cows to be dried off early. Withholding milk from a few cows with high SCCs can have a dramatic impact on the BTSCC.

A more comprehensive strategy is preferred for controlling mastitis for the following reasons: (1) it is a more practical approach, (2) it advocates adoption of management practices applicable to most herds without knowledge of specific pathogens or prevalence of mastitis in herds, (3) this strategy involves conscientious application of only a few basic practices, and (4) success of this strategy has been well documented. This approach is geared toward reducing the rate of new infections and shortening the duration of existing infections. The success of this program has been proven repeatedly and documented extensively throughout the world and consists of effective milking hygiene, proper milking machine function, pre- and postmilking teat disinfection, lactation therapy, antibiotic dry cow therapy, and culling.

Contagious mastitis pathogens are controlled effectively by procedures that prevent spread of bacteria at milking time, which include good udder hygiene, and premilking and postmilking teat disinfection with effective teat disinfectants. In the U.S., the general recommendation is that all quarters of all cows be infused with antibiotics approved for use in nonlactating cows after the last milking of lactation to eliminate existing infections and to prevent new infections during the early dry period, during which the udder is highly susceptible to new infection. It may be necessary to cull chronically infected cows.

Control of environmental mastitis pathogens is best achieved by maintaining a clean, dry environment for lactating and nonlactating cows. Premilking and postmilking teat disinfection is recommended. Antibiotic dry cow therapy is recommended also. Dry cow therapy helps control new infections during the early dry period caused by environmental streptococci. However, dry cow therapy has little effectiveness in controlling coliforms and is not effective in preventing new infections that occur near calving. Vaccines to reduce the severity and duration of coliform mastitis are available and are useful in herds with environmental mastitis.

Current Methods of Mastitis Prevention and Control: Because of the large number of pathogens capable of causing mastitis and the fact that these pathogens behave quite differently, a one-size-fits-all approach to mastitis management is not feasible. Paying attention to the small details described above will continue to be important in every mastitis control program. Since pathogenic bacteria gain entrance into the mammary gland through the teat canal, the greater the bacterial load at the teat end, the greater the probability of an infection occurring, thus emphasizing the importance of maintaining a clean, dry environment and udder hygiene at milking time. Any procedure that reduces the number of bacteria to which the teat end is exposed will likely be beneficial. Proper milking hygiene and good milking practices consist of the following elements: (1) milk in a clean, stress-free environment; (2) check foremilk and udder for signs of clinical mastitis; (3) minimize use of water in the milking parlor; (4) wash teats with warm sanitizing solution, if necessary; (5) apply premilking teat disinfection; (6) dry teats thoroughly 30 to 45 seconds after premilking teat disinfectant application; (7) attach teat cups within one minute after cleaning; (8) provide stable vacuum at claw during peak milk flow; (9) avoid squawking or slipping of teat cup liners during milking; (10) adjust milking units as necessary, (11) shut off vacuum before removing machine; and (12) apply postmilking teat disinfectant shortly after milking machine removal.

Premilking Teat Disinfection: Premilking teat disinfection has been adopted by several dairy producers and is intended to combat environmental pathogens that may have been transmitted to the teat at some point after the last milking. Studies have shown that premilking teat disinfection in combination with postmilking teat disinfection was more effective in preventing new infections than postmilking teat disinfection only. Premilking teat disinfection appears to be effective against environmental pathogens and may also influence contagious pathogens. Dairy producers using this mastitis control procedure must make sure that the premilking teat disinfectant is removed from teats before milking to prevent contamination of milk. There are several good teat disinfectants on the market. However, when choosing a teat disinfectant, require the sales representative to provide evidence that the product is safe, effective, and registered. Furthermore, make sure that manufacturer’s recommendations are followed. Finally, do not assume that all postmilking teat disinfectants would be effective as a premilking teat disinfectant. The NMC publishes a summary of peer-reviewed publications on efficacy of premilking and postmilking teat disinfectants updated annually with information that may be useful to dairy advisers and producers when making decisions on teat disinfectants (

Postmilking Teat Disinfection: Postmilking teat disinfection has been shown repeatedly to be an effective technique for preventing new IMI during lactation. This procedure destroys mastitis pathogens on teats after milking. In general, effective postmilking teat disinfectants reduce the rate of new infection by 50% or more when used in conjunction with other components of mastitis control. Postmilking teat disinfection has been adopted widely in major milk-producing countries throughout the world as an essential part of mastitis control programs. However, postmilking teat disinfection is generally not as effective in preventing new IMI by environmental pathogens such as coliforms and Strep. uberis. This may be due to decreased germicidal activity in the period between milkings. For this reason, efforts have been made to examine premilking teat disinfection and to develop barrier-type teat dips to prevent new IMI by environmental pathogens during the intermilking interval.

Barrier Teat Dips: Barrier-type teat dips were developed with the goal of reducing exposure of teat ends to environmental pathogens during the intermilking period. Barrier dips are generally more viscous. However, their efficacy for prevention of environmental mastitis pathogens is unclear. The incidence of new IMI actually increased with some barrier-type teat disinfectants when evaluated under conditions of experimental challenge with Strep. agalactiae and Staph. aureus. Persistent barrier-type dips have also been used to prevent mastitis during the early dry period and near calving when cows are at high risk for new IMI. One problem has been lack of persistence of the barrier on teat ends.

Antibiotic Therapy of Clinical Mastitis: Despite mastitis control measures such as pre- and postmilking teat disinfection and good hygiene at milking time, mastitis does occur and often requires antibiotic treatment. Antibiotic therapy of clinical mastitis involves: (1) detection of the infected quarter, (2) prompt initiation of treatment, (3) administration of the full series of recommended treatments, (4) maintaining a set of treatment records, (5) identification of treated cows, and (6) making sure the milk is free of antibiotic residues before adding to the bulk tank.

There has been and continues to be concern over the low efficacy of antibiotic therapy against certain mastitis pathogens. This is due to bacterial factors, pharmacologic and pharmacokinetic limitations, and pathobiologic circumstances of the infected mammary gland. Many of these factors appear to be beyond human manipulation for improved therapeutic efficacy, but there are some areas in which work could be done to enhance selection of appropriate antibiotics for therapy.

Efficacy of mastitis therapy is extremely low for chronic Staph. aureus infections; ß-lactamase production may be partly responsible for the low cure rate. However, even with antibiotics to which the bacteria were sensitive in vitro, the cure rate was still low. This suggests the presence of some other mechanisms that interfere with therapy such as formation of microabscesses in mammary tissues and internalization into phagocytic and epithelial cells. Most antibiotics used in mastitis therapy do not penetrate into the infected area and have poor intracellular penetration. Pirlimycin has been studied extensively to treat cows with chronic Staph. aureus IMI because of its lower minimum inhibitory concentration and its tissue-penetrating property. Extended therapy with pirlimycin greatly improved the cure rate against chronic Staph. aureus IMI during lactation. Other results have shown that extended therapy with pirlimycin is an effective procedure for treatment of chronic environmental Streptococcus species (Strep. uberis and Strep. dysgalactiae) IMI in lactating dairy cows. Researchers have also had much success with extended therapy using ceftiofur hyrochloride for treatment of cows with naturally occurring subclinical mastitis and experimentally induced clinical Strep. uberis mastitis.

It is still controversial whether to treat or not treat cows with coliform mastitis. Clinical signs of coliform mastitis are mainly due to the effects from endotoxin. There are few antibiotics suitable for treating cows with coliform mastitis; however, ceftiofur hydrochloride has good in vitro activity against a wide variety of Gram-negative mastitis pathogens and could prove useful for intramammary treatment of cows with clinical mastitis due to Gram-negative mastitis pathogens.

When treating cows with clinical or subclinical mastitis, dairy producers must recognize that administration of antibiotics in a manner inconsistent with the label instruction is considered extra-label use and MUST be carried out under the supervision of the herd veterinarian. Furthermore, milk and meat for human consumption from antibiotic-treated cows must be free of drug residues.

Dry Cow Antibiotic Therapy: The importance of the dry period in the control of mastitis in dairy cows has been recognized for more than 50 years. A classic study by Neave et al. (1950) demonstrated that udders were markedly susceptible to new IMI during the early dry period. The rate of new infection during the first 21 days of the dry period was over six times higher than the rate observed during the previous lactation. Subsequent studies have also shown that udders are highly susceptible to new IMI near calving. Increased susceptibility to new IMI is likely associated with physiological transitions of the mammary gland either from or to a state of active milk production. Many IMI that occur at this time persist throughout the dry period and are often associated with clinical mastitis after calving. Thus, the early dry period was identified as an extremely important time for the control of mastitis in dairy cows.

Most dairy advisers recommend that all quarters of all cows be infused with antibiotics approved for use in dry cows following the last milking of lactation. The objectives of dry cow therapy are twofold: (1) to eliminate infections present during late lactation, and (2) to prevent new infections during the early dry period when mammary glands are highly susceptible to new IMI.

Antibiotic therapy at drying off plays an important role in the control of mastitis during the dry period. Dry cow therapy is particularly effective against streptococci and to a lesser extent against Staph. aureus. Studies have demonstrated that antibiotic therapy at drying off reduced the rate of new environmental streptococcal infection during the early dry period only and that the rate of new coliform IMI was not affected at all. Thus, two significant limitations of present antibiotic formulations used for dry cow therapy are: 1) ineffectiveness against coliform bacteria, which can cause a high proportion of IMI during the early dry period and near calving, and 2) ineffectiveness in preventing new IMI by a broad spectrum of mastitis pathogens during the period near calving when mammary glands are highly susceptible to new infection.

Dry cow antibiotic preparations are formulated primarily to maintain persistent activity during the early dry period and most likely provide little protection during the late dry period. Using the Bacillus stearothermophilus disc assay to detect antibiotic residues, it was demonstrated that dry cow antibiotics persisted for only 14 to 28 days after infusion, and some persisted for shorter periods. Thus, based upon present methods of formulation, it would appear that antibiotic preparations currently available for use in dry cows will not control IMI that occur during the late dry period based on a dry period length of 6 to 8 weeks.

Experimental evidence suggests that dry cow therapy is effective in controlling IMI due to Strep. agalactiae and somewhat effective against Staph. aureus. However, dry cow therapy appears to be less effective against streptococci other than Strep. agalactiae and ineffective against coliform bacteria. Differences in effectiveness of dry cow antibiotic therapy to prevent new IMI are most likely related to several factors. Strep. agalactiae and Staph. aureus are thought to be transmitted primarily during the milking process, and transmission can be controlled by hygiene and antibiotic therapy. The sources of these two organisms are infected mammary glands, colonized teat ducts, and teat lesions. Extramammary sources of contagious mastitis pathogens have been identified but appear to be relatively unimportant in the pathogenesis of infection. Thus, exposure of mammary glands to contagious pathogens during the dry period is reduced in the absence of regular milking, and therapy at drying off tends to control these pathogens effectively.

Heifer Mastitis: Mastitis in breeding age and pregnant heifers is much higher than previously thought. Many IMI in heifers can persist for long periods of time, are associated with elevated somatic cell counts (SCC), and may impair mammary development during gestation and affect milk production after calving. Presence of mastitis before calving increased the risks of infection during lactation, clinical mastitis in the first week after calving, and further cases of mastitis and culling during the first 45 days of lactation.

Mastitis in heifers can be a significant problem for dairy producers. Prepartum intramammary antibiotic infusion of heifer mammary glands was shown to be an effective procedure for eliminating many IMI in heifers during late gestation and for reducing the prevalence of mastitis in heifers both during early lactation and throughout lactation. Data are equivocal regarding the influence of antibiotic treatment of heifers before or near calving on milk production in the subsequent lactation. Some studies reported that prepartum antibiotic-treated heifers produced significantly more milk than control heifers. Conversely, other studies have shown that antibiotic treatment of heifers before or near calving reduced IMI but did not increase milk production or lower SCC in the subsequent lactation. Reasons for this are unclear and need to be delineated. One potential explanation for differences or lack thereof in milk production following prepartum antibiotic therapy could be due to the prevalence of infection in the herds evaluated. For example, one study indicated that prepartum antibiotic treatment of heifers was beneficial on high prevalence (HP) farms but not on low prevalence (LP) farms. This study was conducted in 13 Dutch dairy farms where 196 heifers were treated with cloxacillin 8 to 10 weeks before expected calving and another 196 heifers served as untreated controls. Farms with <15% of heifers with a cow SCC >150,000 cells/ml at the start of the trial were considered low prevalence (LP), while farms with >15% were considered as high prevalence farms (HP). Expected 305-day milk production was significantly higher (496 liters) in antibiotic-treated heifers from HP farms in comparison with untreated animals, but this difference was only 77 liters (not significant) in heifers from LP farms. In both groups of farms, cow SCC was significantly lower in antibiotic-treated heifers compared to untreated controls. An IMI had a significant influence on milk production and cow SCC in the treated and also in the untreated group in comparison to animals without an IMI. Authors concluded that treatment of heifers is beneficial on HP but not on LP farms. Thus, treatment of heifers in a high prevalence herd may be more advantageous from a milk production perspective than in lower prevalence herds. However, high and low prevalence herds still need to be defined.

Although much has been learned about mastitis in heifers, many issues remain unanswered such as: (1) identification of herds where this strategy would be most advantageous and cost effective, (2) whether all heifers in the herd should be treated or only certain heifers, (3) whether certain bacteria are more problematic than others, and (4) identification of key risk factors that could have a significant impact on prevention of heifer mastitis so that antibiotic treatment could be minimized. Additional studies are needed to address these fundamentally important questions.

Use of antibiotics in heifers and cows at times when udders are infected or most susceptible to new IMI is a sound management decision and a prudent use of antibiotics on the farm. Strategies involving prudent use of antibiotics encompass identification of the pathogen causing the infection, determining the susceptibility/resistance of the pathogen to determine the most appropriate antibiotic to use for treatment, and a long enough treatment duration to ensure effective concentrations of the antibiotic to eliminate the pathogen. It is clear that the goal of mastitis therapy should be to eliminate the pathogen causing the infection. Currently, many dairy producers evaluate treatment success based on return of milk and/or the udder to normal. If pathogens causing IMI are eliminated, the opportunity for that pathogen to develop antimicrobial resistance is eliminated.

Internal Teat Sealants: Use of internal teat sealants is a relatively new concept, and much of the early data came from studies conducted in New Zealand. Results of those studies showed that internal teat sealants were effective in preventing new IMI during the dry period, thus improving milk quality in early lactation. A total of 528 cows in late lactation with SCC <200,000 cells/ml were identified in three commercial herds. Of these, bacteriological examination showed 482 cows were uninfected in all four quarters and 46 were infected in only one quarter. At drying off, uninfected quarters were allocated randomly to the following treatments: no infusion (negative controls), infusion with a bismuth subnitrate-based teat sealer, infusion with teat sealer plus antibiotic, or infusion with a cephalonium-based dry cow antibiotic (positive control). New infections were identified during the dry period by periodic udder palpations and at calving by bacteriological culture. All three treatments reduced the incidence of new IMI due to Strep. uberis, both during the dry period and at calving, by about 90%. The majority of infections were due to Strep. uberis. For all treatments, a 50% lower incidence of clinical mastitis over the first five months of the ensuing lactation was reported by farmers. X-ray imaging of 19 teats showed that the teat sealer material was retained, at least in part, in the lower teat sinus over about 100 days of the dry period. The internal teat sealant was as effective in reducing new dry period infections as the infusion of a long-acting dry cow antibiotic formulation. The lower incidence of new infections in the ensuing lactation among the infused quarters implies that fewer subclinical infections persisted from the dry period. Use of teat sealers at drying off appears to offer the same prophylactic efficacy as the dry cow antibiotic approach, and they are apparently quite popular in organic dairy herds.

However, internal teat sealants do not contain antimicrobials and therefore will not eliminate IMI that are present during late lactation. The internal teat sealant in combination with antibiotics would be necessary if cows are infected during late lactation. There have also been some problems reported about sealant residues in milk following calving which apparently can impact cheese production.

Advances in Mastitis Vaccine Research: Given today’s public health and food safety concerns regarding antimicrobial resistance and antibiotic residues in dairy products associated with treatment of diseases like mastitis, approaches to enhance the cow’s immunity to prevent udder disease, improve milk quality, and thus minimize use of antibiotics has gained considerable attention. Yet, for a variety of reasons, vaccines developed for the prevention and control of mastitis have achieved only limited success. The multiplicity of pathogens capable of causing mastitis and knowledge of mammary gland immunology, bacterial virulence factors, and mechanisms of pathogenesis are factors that have hindered development of effective mastitis vaccines. However, some progress has been made in these areas in the last decade or so.

Staphylococcus aureus: Most of the early vaccine research focused on Staph. aureus, and vaccines were based on bacterins derived from bacteria grown in vitro. As our knowledge of bacterial virulence factors increased, different approaches to vaccine formulation have been attempted. The Australians developed a Staph. aureus mastitis vaccine consisting of killed bacteria bearing pseudocapsule and toxoided exotoxins. A large field trial involving 1,819 cows and heifers from seven dairy herds was conducted. The vaccine was administered to pregnant heifers twice during the last trimester of pregnancy and to cows at the end of lactation and again 4 to 6 weeks later. Differences in the incidence of clinical mastitis and prevalence of subclinical mastitis between vaccinated and controls animals were not significant for the whole population of cows and heifers. However, the vaccine was efficacious in reducing the incidence of clinical mastitis and prevalence of subclinical mastitis in one herd that had a serious staphylococcal mastitis problem. The Norwegians tested a vaccine containing whole-inactivated Staph. aureus with pseudocapsule, and α- and β-toxoids in heifers. Results of that study showed a potential protective effect on general udder health of this vaccine during the entire first lactation period. A Louisiana study suggested a positive effect of vaccination with a polyvalent Staph. aureus vaccine by increasing antistaphylococcal antibody titers and in preventing new Staph. aureus infections when the program was initiated at an early age in heifers from a herd with a high exposure to Staph. aureus. More recently, a study in Virginia reported that the percentage of heifers with Staph. aureus IMI at calving was significantly lower in heifers vaccinated with a commercially available vaccine containing a lysed culture of polyvalent Staph. aureus somatic antigens containing five phage types than in unvaccinated heifers. SCCs were also lower in vaccinated heifers during the first week of lactation.

At the USDA, researchers randomly sampled the national herd and found that three Staph. aureus capsule serotypes were responsible for 100% of bovine Staph. aureus mastitis in the U.S. They formulated a vaccine using the three serotypes and tested its ability to cure chronic Staph. aureus infections. In preliminary field trials, the trivalent Staph. aureus vaccine with antibiotics was as effective as the autogenous vaccine with antibiotics for curing chronic Staph. aureus infections. This would allow for treatment of cows chronically infected with Staph. aureus without the necessity of preparing a herd-specific vaccine. Further testing is being conducted to determine the effect of duration of infection on cure rate.

Escherichia coli: An interest in vaccines against environmental mastitis pathogens has been growing. Results obtained with bacterins prepared from the J5 mutant strain of E. coli (O111:B4), referred to as E. coli J5 vaccine, have been encouraging. This mutant is an epimerase-negative strain in which a terminal sugar is absent from the lipopolysaccharide moiety of the cell wall and the lipid A determinant is thus exposed. Trials in California showed that the J5 vaccine reduced clinical coliform mastitis by up to 80% during the first 100 days of lactation. Research in Ohio reported that E. coli J5 vaccine did not prevent IMI but did reduce severity of clinical symptoms following experimental challenge with a heterologous E. coli strain. In addition, a field trial demonstrated that percentage of quarters infected at calving with Gram-negative bacteria did not differ between vaccinated and control cows. However, the vaccine reduced incidence of clinical mastitis; 67% of Gram-negative infections detected at calving in control cows resulted in clinical mastitis during the first 90 days of lactation compared with 20% in vaccinated cows. These data indicate that this vaccine does not prevent new Gram-negative IMI but does reduce the severity of the disease.

Streptococcus uberis: Streptococcus uberis is an important cause of mastitis in dairy cows, particularly during the dry period, the period around calving, and during early lactation that is not controlled effectively by current mastitis control practices. Many Strep. uberis IMI that originate during the nonlactating period, and near calving result in clinical and subclinical mastitis during early lactation. Control programs for reducing Strep. uberis IMI should focus on periods adjacent to the nonlactating period where opportunities exist to develop strategies to reduce the impact of Strep. uberis infections in the dairy herd. The recent discovery and research into a novel protein produced by Strep. uberis, referred to as Streptococcus uberis Adhesion Molecule or SUAM, suggests that it may play a critical role in the pathogenesis of streptococcal mastitis and appears to be a promising vaccine candidate for the prevention of mastitis in dairy cows. Vaccination of dairy cows at drying off, during the mid-dry period and near calving with recombinant SUAM (rSUAM) increased antibody titers in serum at times when the udder is highly susceptible to mastitis. Serum antibodies to rSUAM blocked adherence to, and internalization of, the homologous and hererologous strain of Strep. uberis into bovine mammary epithelial cells. Anti-SUAM antibodies were also found in colostrum of vaccinated cows. Results suggest that vaccination of dairy cows with rSUAM induced a specific antibody capable of blocking and/or interfering with the early pathogenic processes of Strep. uberis IMI.

Culling of Chronically Infected Cows: Culling is an extremely important component of every mastitis control program. Cows not responding favorably to treatment that continue to flare up with clinical mastitis should be culled. In addition, cows with consistently high SCC should be monitored closely. Their continued presence in the herd likely results in other cows becoming infected, especially if cows are chronically infected with contagious mastitis pathogens such as Staph. aureus.

Issues Associated with Antimicrobials: Antibiotics are used extensively in food-producing animals to combat disease and to improve animal performance. On dairy farms, antibiotics such as penicillin, cephalosporin, streptomycin, and many others are used for treatment and prevention of mastitis caused by a variety of Gram-positive and Gram-negative bacteria. Antibiotics are often administrated routinely to entire herds to prevent mastitis during the nonlactating period. Benefits of antibiotic use include decreased pathogen loads, a lower incidence of disease, and a better quality product for human consumption. In contrast to these benefits, however, are suggestions that agricultural use of antibiotics may be partly (largely) responsible for the emergence of antimicrobial-resistant bacteria, which in turn may decrease the efficacy of similar antibiotics used in human medicine to treat diseases of humans. In addition, the risk of antibiotic residues in raw milk is not only a public health issue but an important economical factor for the producer who gets penalized for adulterated milk and for the milk processing plant which jeopardizes the manufacture of dairy foods by processing adulterated milk.

Dairy Food Safety Issues: One area that up until recently has received little attention but is extremely important is pre-harvest dairy food safety. Milk and products derived from milk of dairy cows can harbor a variety of microorganisms and can be important sources of foodborne pathogens. The presence of foodborne pathogens in milk is due to direct contact with contaminated sources in the dairy farm environment and to excretions from the udder of an infected animal. Most milk is pasteurized, so why should the dairy industry be concerned about the microbial quality of bulk tank milk? There are several valid reasons including: (1) outbreaks of disease in humans have been traced to the consumption of unpasteurized milk and have also been traced back to pasteurized milk; (2) unpasteurized milk is consumed directly by dairy producers, farm employees and their families, neighbors, and raw milk advocates; (3) unpasteurized milk is consumed directly by a large segment of the population via consumption of several types of cheeses manufactured from unpasteurized milk; (4) entry of foodborne pathogens via contaminated raw milk into dairy food processing plants can lead to persistence of these pathogens in biofilms and subsequent contamination of processed milk products and exposure of consumers to pathogenic bacteria; (5) pasteurization may not destroy all foodborne pathogens in milk; and (6) inadequate or faulty pasteurization will not destroy all foodborne pathogens. Furthermore, pathogens such as Listeria monocytogenes can survive and thrive in post-pasteurization processing environments. thus leading to recontamination of dairy products. These pathways pose a risk to the consumer from direct exposure to foodborne pathogens present in unpasteurized dairy products as well as dairy products that become re-contaminated after pasteurization. Current data support the model in which the presence of pathogens depends on ingestion of contaminated feed followed by amplification in bovine hosts and fecal dissemination in the farm environment. The final outcome of this cycle is a constantly maintained reservoir of foodborne pathogens that can reach humans by direct contact, ingestion of raw contaminated milk or cheese, or contamination during the processing of milk products. Isolation of bacterial pathogens with similar biotypes from dairy farms and from outbreaks of human disease substantiates this hypothesis.


Production of maximum quantities of high-quality milk is an important goal of every dairy operation. On the other hand, poor milk quality affects all segments of the dairy industry, ultimately resulting in milk with decreased manufacturing properties and dairy products with reduced shelf life. One important measure of milk quality is the number of somatic cells in milk. Milk with a high SCC is produced by cows with mastitis and is of inferior quality. SCC limits for raw milk to be acceptable at dairy processing plants may decrease to levels much lower than they are now, making it increasingly problematic for dairy producers to meet these higher standards. Production of better-quality milk will place a much greater emphasis on strategies for the prevention and control of mastitis to reduce the number of somatic cells in milk. Effective milking-time hygiene, proper milking machine function, pre- and postmilking teat disinfection, lactation therapy, antibiotic dry cow therapy, and culling of chronically infected cows are time-tested management strategies for controlling mastitis and are used extensively throughout the world. Advances in biotechnology have brought exciting new technologies that can/will be used to solve complex problems confronting animal agriculture. New developments, approaches, strategies, and advances in mastitis diagnosis, treatment, and prevention will dramatically improve dairy herd health programs and result in production of maximum quantities of high-quality milk at lower costs. A safe, wholesome, abundant, and nutritious milk supply should be the goal of every dairy producer in the world. Use of effective mastitis control strategies will help dairy producers achieve these important goals.

Author Information

Stephen P. Oliver
The University of Tennessee

Selected References

Barbano, DM, Ma, Y, and Santos, MV. 2006. Influence of raw milk quality on fluid milk shelf life. J. Dairy Sci. 89:E15-E19.

Gillespie, BE, Moorehead H, Dowlen HH, Johnson DL, Lamar KC, Lewis MJ, Ivey SJ, and Oliver SP. 2000. Efficacy of extended pirlimycin therapy for treatment of chronic environmental Streptococcus species intramammary infections in lactating dairy cows. Veterinary Therapeutics 3:373-380.

Godden S, Rapnicki P, Stewart S, Fetrow J, Johnson A, Bey R, and Farnsworth, R. 2003. Effectiveness of an internal teat seal in the prevention of new intramammary infections during the dry and early lactation periods in dairy cows when used with a dry cow intramammary antibiotic. J. Dairy Sci. 86:3899-3911.

Gonzalez RN, Cullor JS, Jasper DE, Farver TB, Bushnell RB, and Oliver MN. 1989. Prevention of clinical coliform mastitis in dairy cows by mutant Escherichia coli vaccine. Can. J. Vet. Res. 53:301.

Hogan JS, Smith KL, Todhunter DA, and Schoenberger PS. 1992b. Field trial to determine efficacy of an Escherichia coli J5 mastitis vaccine. J. Dairy Sci. 75:78-84.

Jayarao BM. 1999. A study on the prevalence of pathogens in bulk tank milk. pp. 148-149 In: Proc. NMC.

Middleton JR, Timms LL, Bader GR, Lakritz, Luby CD, and Steevens BJ. 2005. Effect of prepartum intramammary treatment with pirlimycin hydrochloride on prevalence of early first-lactation mastitis in dairy heifers. J. Am. Vet. Med. Assoc. 227:1969-1974.

Miller, RH, Norman HD, and Thornton LLM. 2008. Somatic cell counts of milk from Dairy Herd Improvement herds during 2007. USDA AIPL Research Report SCC8 (2-07)

NMC. 2008. Summary of peer-reviewed publications on efficacy of premilking and postmilking teat disinfectants published since 1980. pp. 258-272 In: Proc. NMC.

Neave FK, Dodd FH, and Henriques E. 1950. Udder infections in the “dry period.” J. Dairy Res. 17:37.

Nickerson SC, Owens WE, and Boddie RL. 2000. Efficacy of a Staph. aureus mastitis vaccine in dairy heifers. pp. 426-431 In: Proc. Symp. Immunol. Ruminant Mammary Gland, Stresa, Italy.

Nordhaug ML, Nesse LL, Norcross NL, and Gudding R. 1994. A field trial with an experimental vaccine against Staphylococcus aureus mastitis in cattle. 1. Clinical parameters. J. Dairy Sci. 77:1267-1275.

Oliver SP. 1988. Frequency of isolation of environmental mastitis-causing pathogens and incidence of new intramammary infection during the nonlactating period. Am. J. Vet. Res. 49:1789-1793.

Oliver SP, and Mitchell BA. 1984. Prevalence of mastitis pathogens in herds participating in a mastitis control program. J. Dairy Sci. 67:2436-2440.

Oliver SP, Jayarao BM, and Almeida RA. 2005b. Foodborne pathogens in milk and the dairy farm environment: food safety and public health implications. Foodborne Pathogens and Disease 2:115-129.

Philpot WN, and Nickerson SC. 1991. Mastitis: Counter Attack – A Strategy to Combat Mastitis. Published by Babson Bros. Co., Naperville, IL.

Smith KL, Todhunter DA, and Schoenberger PS. 1985a. Environmental pathogens and intramammary infection during the dry period. J. Dairy Sci. 68:402-417.

Timms L. 2000. Field trial evaluations of a persistent barrier teat dip for preventing mastitis during the dry period. pp. 201-202 In: Proc. Symp. Immunol. Ruminant Mammary Gland, Stresa, Italy.

Watson DL, McColl ML, and Davies HI. 1996. Field trial of a staphylococcal mastitis vaccine in dairy herds: clinical, subclinical and microbiological assessments. Aust. Vet. J. 74:447-450.

Woolford MW, Williamson JH, Day AM, and Copeman, PJ. 1998. The prophylactic effect of a teat sealer on bovine mastitis during the dry period and the following lactation. N. Z. Vet. J. 46:12-19.