Mastitis in Cattle

ByMatthias Wieland, DVM, PhD, Dipl.ECBHM
Reviewed/Revised May 2024
Recently Added

With few exceptions, mastitis occurs when microbes enter the teat via the teat canal. Almost any microbe can opportunistically invade the teat canal and cause mastitis. However, most infections are caused by various species of streptococci (or similar gram-positive cocci), staphylococci, and gram-negative rods, especially lactose-fermenting organisms of enteric origin, commonly termed coliforms.

From an epidemiological standpoint, the primary reservoirs of infection for most pathogens may be regarded as contagious or environmental, although this separation can be ambiguous for some pathogens. (See also Udder Diseases in Cattle.)

Except for Mycoplasma spp, which may spread from cow to cow through aerosol transmission and invade the udder subsequent to bacteremia, contagious spread of pathogens occurs during milking, through such pathways as milkers’ hands or the liners of the milking unit. Pathogens that primarily use this mode of transmission include the following:

  • Staphylococcus aureus

  • Streptococcus agalactiae

  • Corynebacterium bovis

Most other pathogens are opportunistic invaders from the cow’s environment, although other streptococci and staphylococci may also have a contagious component.

In addition, contagious transmission may infrequently occur for pathogens typically associated with environmental reservoirs, either through the development of host-adapted virulence factors (as for Escherichia coli) or by shedding of overwhelming numbers of bacteria from infected udders (as for Trueperella [formerly Arcanobacterium] pyogenes and Lactococcus spp). Contagious transmission has also been identified as a possible means of infection for the alga Prototheca zopfii.

The bedding used to house cattle is the primary source of environmental pathogens; however, contaminated teat dips, intramammary infusions, water used for udder preparation before milking, water ponds or mud holes, skin lesions, teat trauma, and flies have all been incriminated as sources of infection.

Based on the presence or absence of clinical signs, mastitis can often be described as subclinical or clinical mastitis.

Subclinical mastitis is the presence of an infection without apparent local inflammation or systemic involvement, although transient episodes of abnormal milk may appear. If the infection persists for at least two months, the infection is termed chronic. Once established, many of these infections persist for entire lactations or the life of the cow, although this varies with the causative pathogen.

Detection of subclinical mastitis is best done by testing milk for somatic cell counts (SCCs; predominantly leukocytes) using either the California Mastitis Test or automated methods provided by dairy herd improvement organizations. SCCs are positively correlated with the presence of infection. Inflammatory changes and decreases in milk quality may start with SCCs as low as 100,000 cells/mL.

Although variable (especially if determined on a single analysis), an SCC ≥ 200,000 cells/mL in a cow indicates a high likelihood of infection. Likewise, the higher the SCC in a herd bulk tank, the higher the prevalence of infection in the herd. Herd SCCs < 200,000 cells/mL are considered desirable (see milk loss and SCC figure).

Milk production decreases in cows with subclinical mastitis. The loss of milk from inflammation is directly proportional to the individual cow SCC; as SCC rises, milk production decreases. These losses can be especially consequential if infection occurs in early lactation and persists as a chronic infection throughout lactation.

Clinical mastitis is an inflammatory response to infection causing visibly abnormal milk (eg, color, fibrin clots). As the extent of the inflammation increases, changes in the udder (swelling, heat, pain, redness) may also be apparent.

  • Cases that include only local clinical signs are referred to as mild or moderate.

  • If the inflammatory response includes signs of systemic involvement (fever, anorexia, shock), the case is termed severe.

  • If the onset is very rapid, as often occurs with severe clinical cases, it is termed acute or severe mastitis.

More severely affected cows tend to have serous secretions in the affected quarter.

Although any number of quarters can be infected simultaneously in subclinical mastitis, typically only one quarter will display clinical mastitis. However, it is not uncommon for clinical episodes caused by Mycoplasma spp to affect multiple quarters.

Gangrenous mastitis can also occur, particularly when subclinical, chronic infections of S aureus become severe at times of immune dysfunction (eg, at parturition). As with subclinical mastitis, culture of milk samples collected from affected quarters is the only reliable method to determine the etiology of clinical cases.

Subclinical Mastitis

Epidemiology of Subclinical Mastitis in Cattle

All dairy herds have cows with subclinical mastitis; however, prevalence of infected cows varies from 5% to 75%, and quarters from 2% to 40%. Many different pathogens can establish a chronic infection in which clinical signs of mastitis will manifest only occasionally.

Historically, subclinical mastitis control focused on the contagious pathogens Streptococcus agalactiae and Staphylococcus aureus, as well as other gram-positive cocci, most notably Streptococcus dysgalactiae (which may also be contagious or an environmental pathogen), Streptococcus uberis, enterococci, and numerous other nonaureus staphylococci (previously termed coagulase-negative staphylococci), including Staphylococcus hyicus, Staphylococcus epidermidis, Staphylococcus xylosus, and Staphylococcus intermedius.

Herds have been identified that have considerable subclinical mastitis caused by gram-negative rods such as Klebsiella spp, Serratia marcescens, Pseudomonas aeruginosa, and other atypical pathogens such as Candida spp and Prototheca zopfii. Because of increasing herd size throughout the dairy industry and more movement of cattle between herds and geographic locations, Mycoplasma spp, especially Mycoplasma bovis, have been recognized as frequent pathogens in some herds, with cows exhibiting both subclinical and clinical signs.

For contagious pathogens, adult lactating cattle are most at risk of infection. The primary reservoir of infection is the mammary gland; transmission occurs at milking with either milkers’ hands or milking equipment acting as fomites. Primiparous heifers have been reported to be infected with staphylococci and streptococci before calving, although the prevalence varies greatly among herds and geographic regions. Teat-end dermatitis caused by the horn fly, Haematobia irritans, which can harbor S aureus, has been associated with increased risk of infection in heifers, especially in warmer climates.

For Streptococcus agalactiae, Staphylococcus aureus, and nonaureus staphylococci, there is little or no seasonal variation in the incidence of infection.

Key Performance Indicators of Subclinical Mastitis in Cattle

The most important measure to monitor subclinical mastitis in dairy herds is testing milk for SCCs and the calculation of key performance indicators. These calculations are based on a predefined SCC threshold and the comparison of the cows' SCC over the course of two subsequent testings (see key performance indicators figure).

Internationally, an SCC of 200,000 cells/mL is often considered the threshold for determining infection status.

  • A new infection is defined as an SCC ≥ 200,000 cells/mL at the most recent testing given that the SCC was < 200,000 cells/mL at the previous testing.

  • Percentage of new infections is calculated as the number of cows with a new infection divided by the number of cows in the lactating herd with at least two testings in the current lactation.

  • The new infection risk is calculated as the number of cows with a new infection divided by the number of cows that were not infected (SCC < 200,000 cells/mL) at the previous testing.

  • A cure is defined as an SCC < 200,000 cells/mL at the most recent testing given that the SCC was ≥ 200,000 cells/mL at the previous testing.

  • Percentage cured is calculated as the number of cows that cured divided by the number of cows in the lactating herd with at least two testings in the current lactation.

  • The cure risk is calculated as the number of cows that cured divided by the cows that were infected (SCC ≥ 200,000 cells/mL) at the previous testing.

  • Percentage clean is calculated as the number of cows that had a low SCC (< 200,000 cells/mL) at both the previous and the most recent testing.

  • Percentage chronic is calculated as the number of cows that were infected (SCC ≥ 200,000 cells/mL) at both the previous and the most recent testing.

  • Percentage high fresh is calculated as the number of cows with a high SCC (≥ 200,000 cells/mL) at the first testing after calving divided by the number of cows with a first test SCC after calving.

Commonly used goals are percentage new infections < 8%; new infection risk < 8%; percentage cured greater than percentage new infections; and cure risk > 35%. Dairy producers should strive to achieve a percentage high fresh < 10%.

Treatment of Subclinical Mastitis in Cattle

  • Determine causative agent

  • Antimicrobials

Subclinical mastitis treatment is indicated when treatment costs are expected to be outweighed by production gains after elimination of infection. However, prevention is always preferred to treatment, particularly because lactating glands have compromised immune function and are therefore susceptible to infection. The need to treat subclinical mastitis should be carefully considered based on the causative agent and duration of infection.

In the case of contagious pathogens, elimination may result in a decrease of the reservoir of infection for previously noninfected cows. No noteworthy economic losses will occur as a result of delaying treatment until bacterial culture can be completed. However, many subclinical mastitis cases are chronic, and, particularly in the case of S aureus, prediction of therapeutic outcome by in vitro testing is unreliable. Drug distribution after intramammary administration may not be adequate because of extensive fibrosis and microabscess formation in the mammary gland. Cows with a long duration of infection (> 3 months), more than one quarter infected, or infected with pathogens resistant to antimicrobials typically used in intramammary infusions are likely to be refractory to treatment.

An unusual opportunity for successful treatment of subclinical intramammary infection (IMI) is possible with Streptococcus agalactiae. Prevalence of IMIs caused by this pathogen can be rapidly decreased by treating all the infected cows in a herd with antimicrobials. All four quarters of infected cows should be treated to ensure elimination of the pathogen and to prevent possible cross-infection of a noninfected quarter. Cure rates often range from 75% to 90%.

  • Labeled use of commercial intramammary products that contain amoxicillin, penicillin, or cephalosporins is preferred.

  • It is critical to apply strict aseptic techniques (eg, use of alcohol-soaked pads for teat-end preparation) whenever any intramammary infusion product is administered.

  • Drugs originating from multiple-dose vials (labeled for systemic treatment) should not be used for intramammary treatment, because commercial intramammary preparations have superior quality control standards for sterility and better reliability to predict withholding periods for milk and meat after treatment.

Herds undergoing extensive treatment for S agalactiae must be monitored by use of SCCs and subsequent milk culture to identify cows not treated or cured during the initial treatment. Usually, 30-day monitoring intervals are successful. Teat dipping after milking and treatment of all dry cows are also essential strategies for elimination of S agalactiae from the herd. A small percentage of cows will not respond to treatment and are best segregated or culled.

Most other streptococci also display in vitro susceptibility to numerous antimicrobials, especially beta-lactam antimicrobials. Despite this apparent susceptibility, many streptococcal infections are not as easily cured as those caused by S agalactiae. Generally, subclinical infections caused by S uberis and S dysgalactiae should be treated at the end of lactation with intramammary infusions of commercial dry cow products. Cure rates at this time may exceed 75%. Other streptococcal-like organisms such as Lactococcus spp and Enterococcus spp are often refractory to treatment.

S aureus intramammary infections result in deep-seated abscesses. Treatment is difficult because resistance to antimicrobials (particularly beta-lactam antimicrobials) is more common than with streptococcal infections, and S aureus may survive intracellularly after phagocytosis. Intramammary infusions may cure only 20%–40% of infections, and less for chronic infections.

The success rate of treatment for chronic subclinical mastitis caused by S aureus may be increased by using both parenteral and intramammary treatment. However, systemic treatment involves extra-label drug use, and milk and meat withholding periods must be determined. In addition, treatment should be administered for periods long enough (7–10 days) to allow effective clearance of the pathogen. Dry cow therapy is more economical than lactating cow therapy and avoids the risk of residues in milk.

Occasionally, premature agalactia will occur in chronically infected quarters. Culling may be a practical option for these cows. Alternatively, it is common to dry off the infected quarter and continue to milk the cow. This may have some benefit for genetically superior animals within a herd or for cows that are to be maintained until calving. The goal is to eliminate the infection by causing fibrosis of the affected quarter, thus decreasing the risk of infection for other cows. In addition, such cows will no longer be contributing high-SCC milk (from the infected quarter), thus helping to maintain quality of the marketed milk. Drying off quarters, culling, or treatment as a means to decrease SCC contributions from infected cows is a palliative approach to mastitis control, which is better addressed by the prevention of infections.

Dry Cows

The dry period of the lactation cycle is a critical time for the udder health of dairy cows. The mammary gland undergoes marked biochemical, cellular, and immunological changes. Involution of the mammary parenchyma begins 1–2 days after the end of lactation and continues for 10–14 days. During this time, the gland is particularly vulnerable to new intramammary infections. However, the involuted mammary gland offers the most hostile immune environment for bacterial pathogens. Consequently, the dry period is an ideal time to attain synergy between antimicrobial treatment and immune function, without incurring the extensive costs typical of lactating cow therapy.

Numerous commercial products are available for dry cow treatment and include penicillin, cloxacillin, cephapirin, ceftiofur, and novobiocin. One tube per quarter is sufficient and should be administered immediately after the last milking of lactation. Treatment should not be repeated by intramammary infusion; if there is a perceived need to extend treatment, systemic administration should be used as an adjunct to the intramammary infusion. In addition to eliminating existing subclinical infections, one of the most critical roles of dry cow treatment is to prevent new infections.

Internal teat sealants, as a supplemental infusion after antimicrobial infusions at dry-off, serve as a physical barrier to help decrease new infections. The use of internal teat sealants appears to decrease the incidence of new infections, in comparison to antimicrobial treatment alone. Modern dairy cows have such a high level of milk production at dry-off that their teat canals may remain patent for a long period of time after milking ceases, so infection remains a risk even when they are not lactating. As with lactating cow infusions, it is important to follow strict aseptic technique for any infusion at dry-off.

Blanket dry cow therapy (BDCT; treating all quarters of all cows at dry-off) has been a foundation of mastitis control for more than 50 years. However, despite BDCT's success in preventing and curing IMIs over the dry period, the prevalence of various pathogens has changed over time. Most of the dry cow products target gram-positive cocci, which may not be the predominant pathogens in a particular herd. In addition, advances in housing and bedding, nutritional management, and internal teat sealants have all helped decrease the rate of IMIs during the dry period.

For these reasons, selective dry cow therapy (SDCT; treating only cows that are identified as infected at dry-off) could be considered an alternative to BDCT. The biggest caveat in choosing BDCT versus SDCT is that all herds have unique challenges and management approaches to their operations, so a dry cow therapy program must be tailored to fit their needs.

Herds that struggle with basic mastitis control (bulk tank SCC > 200,000 cells/mL) are not the best candidates for SDCT. In addition, both metrics for outcomes and protocols to select cows for dry cow therapy should be rigorously followed. Herd-specific algorithms should include, at the very least, both clinical mastitis history and individual cow SCCs during the lactation before dry-off (see dry cow SCC figure).

In the US, fewer herds are using dairy herd improvement SCC testing and thus have difficulty monitoring subclinical mastitis. Also, because of greater emphasis on so-called parlor efficiency, ie, the rate of cow throughput in many larger dairies, milking operators may not have time to correctly identify clinical mastitis, let alone strip milk from teats.

As a result, the ability to determine the efficacy of a dry cow therapy program, such as new and cured IMI cases over the dry cow period, and clinical mastitis in the first 30 days in milk (ie, number of cows that experienced one or more cases of clinical mastitis within the first 30 days in milk divided by the number of cows calving) will be tenuous in some herds. Although culture of milk samples, either before drying-off or from clinical cases, is a useful part of any herd mastitis control program, especially for those choosing SDCT, there is reluctance on the part of most dairy producers to use milk cultures. The bottom line for the decision to use SDCT is to ensure that the tools and the willingness are in place to properly select cows and monitor changes in milk quality.


Most IMIs in calving heifers are caused by staphylococcal species other than S aureus, which have a high rate of spontaneous cure. However, under some herd conditions, a substantial portion of heifers have intractable infections, including those caused by S aureus (see gangrenous mastitis image). Potential sources include the milk they were fed as calves and colonization of body sites such as tonsils and skin. There is also a geographic risk factor: fly bite dermatitis of the teat end, which compromises this important physical barrier to infection, may play a role in the pathogenesis.

Intramammary infusions of beta-lactam antimicrobial drugs 7–14 days before expected calving dates have been reported to decrease the prevalence of IMIs at calving. However, longterm benefits on SCCs, milk production, and incidence of clinical mastitis during lactation were found to be highly variable by herd. Strict teat-end antisepsis should be followed before infusion to prevent contamination; thus, the labor to handle animals for treatment can be extensive. This is not a recommended management program for many dairies. However, if herd records indicate that the prevalence of IMIs in first-lactation animals at calving is high (> 20%), particularly with staphylococci, this regimen may be considered.

Prevention of Subclinical Mastitis in Cattle

New subclinical mastitis infections are prevented by focusing management efforts on decreasing the presence of pathogens on the teat end. Thus, clean and dry bedding, clean and dry udders at the time of milking, and not using water during the milking protocols (except to maintain hygiene of milking units), as well as maintaining teat-end health, all have a positive effect on control.

For contagious pathogens, the single most important management practice to prevent transmission of new infections is the use of an effective germicide as a postmilking teat dip. These products should be applied as a dip (rather than a spray) immediately after milking. Other practices that augment teat hygiene include the following:

  • use of individual towels to dry teats

  • gloves for milkers’ hands

  • use of a premilking germicide (spray or dip)

  • attachment of units at the proper time after teat stimulation (60–120 seconds)

  • not overmilking

  • cleaning milking units after an infected cow has been milked

  • segregation of infected cows whenever possible

Routine milking equipment evaluations should be conducted to ensure teat-end vacuum is operating at a proper level and remains stable during milking. Proper pulsator function is critical, and milking liners and rubber air hoses should be replaced as needed.

Recently, a vaccine that targets Klebsiella spp has shown promise for decreasing SCCs (1).

Milking hygiene also decreases the new infection risk of environmental pathogens.

Importantly, cows should be provided dry, clean bedding. Inorganic bedding supports less bacterial growth than cellulose-based material; thus, sand is preferred over sawdust, straw, recycled paper, or manure solids. In particular, a higher incidence of infections caused by Klebsiella spp has been associated with sawdust bedding. However, bacterial numbers can vary greatly depending on moisture and presence of organic matter (such as in sand after recycling). Thus, control of environmental mastitis should not be based solely on the choice of bedding material.

The following are practices that have a positive impact on environmental mastitis control:

  • regular cleaning or changing of bedding

  • decreasing heat stress

  • removing udder hair

  • maintaining healthy teat condition

  • decreasing udder edema in periparturient cows

  • avoidance of areas that accumulate water

  • maintenance of stalls for proper lying behavior

  • preventing frostbite and fly exposure

Clinical Mastitis

Infections from any pathogen can be clinical or subclinical, depending on the duration of infection, host immune status, and pathogen virulence. Control of clinical mastitis usually focuses on prevention and elimination of pathogens that arise from an environmental reservoir. Thus, the epidemiology and prevention of clinical mastitis is similar to control of subclinical mastitis.

Epidemiology of Clinical Mastitis in Cattle

Except for outbreaks of Mycoplasma spp, clinical mastitis in most dairy herds is caused by environmental pathogens. In addition, many clinical mastitis cases are transient, especially those that are initial episodes for a cow and quarter. The assessment of clinical mastitis within a herd is based on incidence (ie, occurrence of new cases over a specified period of time) and not prevalence (ie, total affected animals at a given point in time).

Methods to monitor subclinical mastitis, ie, routine SCCs and culture of cows with increased SCCs, are inconsistent predictors of clinical mastitis cases. Cows with high SCCs caused by chronic infections may occasionally display clinical mastitis, although it is usually mild. However, cows with low SCCs are also prone to developing clinical mastitis.

Cow history from each case (eg, season, age, stage of lactation, and previous episodes) should be recorded to help determine risk factors. Milk samples should be collected from affected quarters and, when feasible, antimicrobial susceptibility testing performed. For well-managed herds in which mastitis caused by contagious pathogens has been controlled, a goal for the incidence of clinical mastitis should be 1–2 cases/100 cows milking/month. Severe mastitis cases should be in the range of 1–2 cases/100 cows milking/year.

Typically, 30%–40% of milk samples collected from clinical mastitis cases yield no organisms on culture. However, of the samples that do yield organisms, 90%–95% of the isolated bacteria include a wide variety of streptococci, staphylococci, or coliforms. If this is not the case, especially if noncoliform, gram-negative rods, mycotic, or algal (Prototheca spp) pathogens predominate, a point source of infection should be considered.

Severe Clinical Mastitis in Cattle

Coliforms (lactose-fermenting gram-negative rods of the family Enterobacteriaceae) are the most common cause of severe clinical mastitis in cattle. Most coliform infections are cleared from the gland with few or mild clinical signs. However, severe mastitis with clinical signs of systemic illness occurs when bacterial concentrations in milk increase enough to stimulate a marked immune response (see milk samples with coliform bacteria image).

Severe mastitis caused by coliforms results in a higher incidence of cow death or agalactia-related culling (30%–50% of cases) than mastitis caused by other pathogens (5%–10% of cases). Prognosis for cases of Klebsiella infection should be particularly guarded because affected cows are twice as likely to be culled or die as those infected by other coliforms. Thus, primary treatment for severe clinical mastitis should be directed against coliform organisms, although secondary consideration must be given for other causative agents.

Supportive care, including fluid therapy, is likely the most beneficial component of the therapeutic regimen. Treatment with antimicrobials is ideally based on identification of the causative pathogen; however, this is not attainable for some hours after initial case recognition. In addition, there are currently no FDA-approved regimens for systemically administered antimicrobial treatment of severe clinical mastitis in the US.

After infection, coliform numbers in milk increase rapidly, often attaining peak concentrations within a few hours. A rapid decline in bacteria follows neutrophil migration into the gland; however, the ensuing inflammatory and systemic changes are caused by release of lipopolysaccharide (LPS) endotoxin from the bacteria and causes an acute phase response (sepsis). By the time treatment is initiated, much of the LPS exposure has occurred. Thus, the primary therapeutic concern is the treatment of endotoxic shock with fluid therapy, electrolytes, and anti-inflammatory drugs. The IV route is preferred as the initial method of fluid administration.

If isotonic saline (0.9% NaCl) solution is administered, 30–40 L is necessary throughout a 4-hour period, which can be difficult under farm conditions. A practical alternative is 2 L of hypertonic saline (7% NaCl) solution administered IV. This induces rapid fluid uptake from the body compartment into the circulation. Cows should then be offered free-choice water to drink, and if at least 30–38 L is not consumed, 19–26 L of water should be pumped into the rumen.

Many cows with endotoxic shock are marginally hypocalcemic; thus, 500 mL of calcium borogluconate should be administered SC (to avoid potential complications of IV administration). Alternatively, rapid absorption calcium gels, designed for periparturient hypocalcemia, can be administered. If the cow remains in shock, continued fluid therapy should be administered PO or IV as isotonic, not hypertonic, fluids.

If administered early in the course of disease, glucocorticoids may be helpful in cases of mastitis caused by endotoxin-producing coliforms. These compounds inhibit many proinflammatory pathways related to the acute-phase response. Administration of dexamethasone (30 mg, IM) to dairy cows immediately after introduction of E coli into the mammary gland has been reported to decrease mammary gland swelling and improve rumen motility. Care should be exercised in administering these drugs to pregnant animals due to the risk of abortion; however, severe clinical mastitis in and of itself may cause pregnancy loss in cattle.

There is little published research on the use of glucocorticoids for mastitis caused by gram-positive bacteria. It is reasonable to expect that cows with gram-positive infections would be less likely to benefit from the anti-inflammatory activities of glucocorticoids and may even be adversely affected. Intramammary glucocorticoid administration to decrease local inflammation has been considered a therapeutic option. Although products that combine antimicrobial and glucocorticoid drugs for intramammary administration exist in Europe, it is not clear whether clinical benefit is gained when compared with antimicrobial treatment alone. As a general guideline, glucocorticoid treatment should be reserved for severe cases of gram-negative mastitis, with a single dose administered early in the disease course.

NSAIDs are widely used in treatment of acute mastitis. Flunixin meglumine, flurbiprofen, carprofen, meloxicam, and ketoprofen have been used as treatments for experimental coliform mastitis or endotoxin-induced mastitis. Systemic use of these drugs is preferred over orally administered aspirin, which is not likely to attain effective concentrations in tissue or lead to beneficial results.

Dipyrone use in food animals is specifically prohibited by the FDA. Phenylbutazone is prohibited in dairy cattle > 20 months old; the tolerance level for phenylbutazone is zero, hence any concentration detected is an illegal residue. Thus, these two drugs should not be used for anti-inflammatory treatment of mastitis in cattle.

Ketoprofen is available as a veterinary product for use in horses, has a high therapeutic index, has favorable pharmacokinetics for use in lactating dairy cattle, and is approved for use in cattle in some countries. However, it is not labeled for food animal use in the US. The Food Animal Residue Avoidance Databank (FARAD) recommends withdrawal intervals of 7 days for slaughter and 24 hours for milk for dosages up to 3.3 mg/kg, IV or IM, every 24 hours for up to 3 days.

Flunixin meglumine (1.1–2.2 mg/kg, IV) is labeled for beef and dairy cattle. It is the only NSAID labeled for use in cattle in the US and is therefore the most logical choice to treat severe clinical mastitis. In a field study, increased survival rate has not been demonstrated after treatment of clinical acute mastitis with flunixin meglumine (2). However, in studies of experimental mastitis, flunixin meglumine decreased the severity of clinical signs such as fever, listlessness, elevated heart and respiratory rates, and udder pain (3, 4).

The FDA-approved withdrawal intervals for flunixin meglumine are 4 days for slaughter and 36 hours for milk when used as labeled by IV administration. Because of extensive and unpredictable withdrawal periods and risk of tissue damage, this drug should not be administered by IM injection. As with the glucocorticoids, NSAIDs may relieve clinical signs and promote well-being. Administration early in the course of infection is likely to increase clinical benefit.

For endotoxic shock, antimicrobial treatment may be of secondary importance relative to immediate supportive care; however, it remains an integral part of a therapeutic regimen.

Occasionally, coliform infections do result in chronic mastitis. Bacteremia occurs in > 50% of severe coliform cases.

Numerous other pathogens, including gram-positive cocci, can also cause severe clinical mastitis and can be difficult to distinguish from cases caused by coliforms.

Selection of an appropriate antimicrobial for the treatment of severe coliform mastitis depends primarily on the susceptibility of the organism to the selected drug and the ability to maintain effective concentrations at the primary pharmacological target (which, in the case of coliform mastitis, is the plasma compartment of the cow).

Oxytetracycline (11 mg/kg, IV, every 24 hours) appears to improve outcome of cows with clinical coliform mastitis (not necessarily severe) as compared with cows that did not receive systemic antimicrobials. Ceftiofur sodium (2.2 mg/kg, IM, every 24 hours) appears to decrease mortality and cull rates of cows with severe coliform mastitis and enhance recovery of milk production. This drug distributes poorly to the mammary gland, supporting the importance of targeting treatment for bacteremia in addition to the mammary gland.

Intramammary infusion of antimicrobials should be administered to cows with severe clinical mastitis. This treatment may not affect the outcome of coliform cases but will likely improve outcomes for cases caused by gram-positive cocci. The need for continued antimicrobial treatment in cows with grossly abnormal milk, but with improved appetite, attitude, and milk production, should be evaluated critically. Unnecessary extension of treatment in these instances results in increased expense due to discarded milk and risks antimicrobial residues in marketed milk.

Mild Clinical Mastitis in Cattle

Microorganisms are not isolated from 30%–40% of bacteriological cultures of milk samples collected from cows with clinical mastitis. Many mild mastitis cases that fail to yield bacteria on culture are coliform intramammary infections that resolve before treatment is necessary. In addition, numerous mild clinical mastitis cases are temporary setbacks in the balance between pathogen and host defenses that occurs in chronic mastitis (see mild clinical mastitis samples image).

Clinical judgment and individual herd history should determine the course of treatment for mild clinical mastitis cases in dairy herds. Use of approved commercial intramammary infusions is the best option. The foundation of success is bacteriological cure but will be more practically based on return to normal milk.

The frequency of relapsed cases should be monitored as the best measure of therapeutic efficacy, because many cases will be deemed to have been successfully treated in the short term but relapse later in lactation. If mastitis recurs regularly in affected quarters in the absence of systemic clinical signs, treatment should not be repeated; the quarter should be dried or the animal should be culled.

In addition, augmentation with parenteral treatment for these cases has not been demonstrated to be effective; any potential therapeutic benefit will not likely overcome the expense of discarded milk, other related treatment costs, and the increased risk of residues in milk and meat. Previous history of clinical cases, long duration of infection (as exhibited by high individual SCCs or extended periods of increased SCCs), and infections caused by nonresponsive pathogens are the greatest risk factors for poor therapeutic outcome.

If standard regimens achieve less than desired results, it would be better to extend the duration of initial treatment rather than change drugs or increase dosage. However, results will vary with the bacteriology of the herd. Care should especially be exercised in aseptic preparation of the teat for extended treatment because of the increased risk of nosocomial infections.

The most efficient use of antimicrobial treatment, and the best option to decrease unnecessary use, is to apply "culture-based treatment" decision-making as part of the therapeutic protocol on a farm (see clinical mastitis protocol figure):

  • Treatment is withheld from an affected quarter (mild clinical mastitis) until results from a bacteriological culture of a milk sample are obtained, usually within 24–48 hours; this amount of time does not adversely impact bacterial cures, relapses, milk production, or SCCs for cows selected for treatment.

  • Culture-dependent treatment decisions may vary from farm to farm; however, in general, antimicrobial treatment does not improve the outcome of cases that yield no organism, gram-negative organisms, or unusual pathogens (eg, Pseudomonas spp).

  • Thus, by excluding cases that yield these culture results, dairy herds can decrease antimicrobial use for mild clinical treatment by 50%–75%.

Simple milk bacteriological analysis that identifies gram-positive from gram-negative pathogens, as well as no isolation, can be performed in veterinary clinics or, with proper training, on the farm. On-farm culture systems are widely used on dairy operations to inform pathogen-based mastitis management and allow for the discrimination of gram-positive, gram-negative, or no bacterial growth. More-sophisticated systems facilitate genus-specific and species-level identification. The implementation of on-farm culture systems has the potential to decrease antimicrobial usage in the dairy industry.

Unusual Pathogens in Clinical Mastitis in Cattle

Pseudomonas aeruginosa may cause outbreaks of clinical mastitis. Generally, a persistent infection occurs, which may be characterized by intermittent acute or subacute exacerbations.

The organism is found in soil-water environments common to dairy farms. Herd infections have been reported after extensive exposure to contaminated wash water in the milking parlor, teat cup liners, or intramammary treatments administered by milkers. Failure to use aseptic techniques for treating udders or use of contaminated milking equipment may lead to P aeruginosa IMI.

Severe peracute mastitis with toxemia and high mortality may occur in some cows, whereas subclinical infections may occur in others. The organism can persist in a gland for multiple lactations; however, spontaneous recovery may occur. Other than supportive care for severe episodes, treatment is of little value. Culling is recommended for persistently clinically affected cows.

Trueperella pyogenes is common in suppurative processes of cattle and pigs and produces a characteristic mastitis in heifers and dry cows. It occasionally infects lactating udders after teat injury, and it may be a secondary invader. The inflammation is typified by the formation of profuse, foul-smelling, purulent exudate.

Mastitis due to T pyogenes is common among dry cows and heifers that are pastured during the summer months on fields and that have access to ponds or wet areas. The vector for animal-to-animal spread is the fly Haematobia irritans. Control of infections is attained by limiting the ability of cows to stand in water and by controlling flies. Treatment is rarely successful, and the infected quarter is usually lost to production. Infected cows may be systemically ill, and cows with abscesses usually should be culled.

Mycoplasma spp can cause a severe form of mastitis that may spread rapidly through a herd with serious consequences. Mycoplasma bovis is the most common cause. Other species include Mycoplasma californicum, Mycoplasma canadense, and Mycoplasma bovigenitalium. Onset is rapid, and the source of infection is often endogenous after outbreaks of respiratory disease in heifers or cows.

The disease often follows herd expansion, in which animals from outside sources have been added. Typically, introduced animals will be subclinically affected carriers and then shed the organism via respiratory or intramammary transmission. Some or all quarters become involved. Loss of production is often dramatic, and the secretion is soon replaced by a serous or purulent exudate. Initially, a characteristic fine granular or flaky sediment may be observed in the material removed from infected glands.

Despite the severe local effects on udder tissue, cows usually do not manifest clinical signs of systemic involvement. The infection may persist through the dry period. Identification of all infected cows in a herd can be difficult because of the frequent propensity of these cows to become subclinical carriers and intermittently shed the organism in milk.

Because there is no satisfactory treatment for mastitis caused by Mycoplasma, affected cows should be segregated during active outbreaks. Routine screening of the bulk tank and milk strings (ie, groups of cows that are housed or milked together) may help identify the presence of infected cows. However, milk culture of cows with clinical mastitis, or recently calved cows, offers the most reliable surveillance.

If cows continue to display clinical mastitis or systemic clinical signs, they should be culled. Sanitary measures should be strictly enforced, especially at milking and in hospital or treatment areas. Milk from Mycoplasma-infected cows should not be fed to calves, because this may result in pneumonia or otitis media.

Nocardia asteroides causes a destructive mastitis characterized by acute onset, high temperature, anorexia, rapid wasting, and marked swelling of the udder. Typically, a granulomatous inflammation of the udder occurs that leads to extensive fibrosis and formation of palpable nodules. This particular infection of the udder may be associated with contamination during intramammary treatment for the more common forms of mastitis. Culling is recommended for infected cows.

Serratia mastitis may arise from contamination of milk hoses, teat dips, water supply, or other equipment used in the milking process. The organism is resistant to disinfectants. Cows with this form of mastitis that continue to display clinical signs should be culled.

Mastitis due to various mycotic organisms (yeasts) has appeared in dairy herds, especially after the use of penicillin in association with prolonged repetitive use of antimicrobial infusions in individual cows. Yeasts grow well in the presence of penicillin and some other antimicrobials; they may be introduced during udder infusions of antimicrobials, multiply, and cause mastitis. However, heifers that have never received intramammary infusions may also develop yeast mastitis. Clinical signs may be severe, with a fever followed either by spontaneous recovery in approximately 2 weeks or, more rarely, by a chronic destructive mastitis. Other yeast infections cause minimal inflammation and are self-limiting. If mastitis due to yeast is suspected, antibacterial treatment should be stopped immediately.

A chronic mastitis similar to that caused by the tubercle bacillus has been reported to be caused by acid-fast Mycobacterium spp derived from the soil, such as Mycobacterium fortuitum, Mycobacterium smegmatis, Mycobacterium vaccae, and Mycobacterium phlei. These organisms are introduced into the gland along with antimicrobials (especially penicillin) in oil or "home remedy" vehicles; they tend to be saprophytic and to disappear from infected quarters, at least by the next lactation. In the meantime, mastitis is usually moderate. Distinct outbreaks do occur and several have been reported, especially with M fortuitum and M smegmatis.

Prototheca spp are nonpigmented unicellular algae commonly found in wet environments such as streams, stagnant ponds, and marine waters, particularly in humid habitats with organic matter in the soil. In dairy farm environments, they are especially abundant in muddy or wet outdoor runs or lots, resting areas, paths where animals are driven, and pastures contaminated with slurry.

Infections during the dry period are possible, especially in cows exposed to manure pack bedding or outside lots. In addition, poor infusion asepsis and use of multidose antimicrobial products not intended for intramammary infusion have been linked to outbreaks. Case reports suggest that should IMIs in a herd reach critical levels, contagious transmission of Prototheca spp during milking may also occur.

Protothecal mastitis in dairy cattle is often chronic; cows appear clinically normal but with increased SCCs in the milk, although sporadic severe infections occur. Infections may spontaneously resolve; however, longterm carriage with intermittent shedding is common. After initially causing clinical mastitis, infections may be undetectable by culture of milk for several months, only to recur during the subsequent lactation, particularly soon after calving. Therapeutic interventions are unrewarding.

Dairy producers have limited ability to predict the progression or affect the outcome of protothecal mastitis and are constrained to management options similar to those used to manage chronic mastitis caused by other pathogens. Therefore, prevention is the primary focus rather than mitigation of infections. To decrease pathogen exposure to other noninfected cows in the herd, chronic mastitis cows are often culled.

The primary causative agent of protothecal mastitis in cattle has been identified as Prototheca zopfii. Other reports have challenged the absolute exclusivity of P zopfii as the etiological agent of protothecal mastitis; however, on a practical basis, cows identified as having mastitis caused by Prototheca spp are managed in similar fashion, regardless of species or genotype. Often, Prototheca spp are misidentified on routine milk culture, so selective media or the use of a Gram stain should be used (see Gram stain in milk smear image).

Mastitis caused by Bacillus spp has much the same origin, clinical signs, and methods of prevention as do other unusual pathogens. As with other organisms in this category, treatment is not generally successful.

Prevention of Clinical Mastitis in Cattle

Prevention of clinical mastitis in cattle is essentially identical to that for subclinical mastitis, ie, decreasing microbe exposure to the teats. Because most clinical mastitis is caused by pathogens that are predominantly environmental in origin, decreasing exposure from bedding, housing, and in outdoor lots and pastures is critical. However, good premilking hygiene to ensure teats are clean and dry before the attachment of the milking unit, including use of germicides (premilking teat dips), is beneficial.

With the exception of bacterins that target gram-negative pathogens, particularly coliforms, immunization to decrease the effects of mastitis has been largely unsuccessful or, at best, variable. Core-antigen technology based on J5 mutant E coli can help decrease the severity of clinical mastitis caused by coliforms. Immunization with these bacterins should include multiple doses during the dry period to decrease the incidence of clinical coliform mastitis frequently associated with early lactation. Protocols for extended numbers of immunizations of these bacterins may be warranted in herds with high rates of severe mastitis beyond 60 days in milk because protection often wanes 50–60 days after the last immunization.

It is important to note that these bacterins decrease the severity of clinical mastitis cases caused by gram-negative pathogens only and that while the severity of clinical signs can be decreased, these bacterins do not prevent infections.

The success of core-antigen bacterins relies on five fundamental principles:

  1. Validate that coliform organisms are the primary cause of severe clinical mastitis in a herd by culture of milk samples.

  2. Determine whether the incidence of severe coliform mastitis is > 1% of the herd each year.

  3. Describe the animals at risk, eg, days in milk and lactation.

  4. Decrease other herd risk factors for coliform mastitis, such as inadequate bedding.

  5. Develop a vaccination protocol that targets animals at risk.

The vaccine with a Klebsiella spp siderophore receptor protein has also shown promise for decreasing the severity of clinical mastitis caused by gram-negative pathogens.

Key Points

  • Bovine mastitis is defined as the inflammation of one or more mammary glands. Most mastitis cases are caused by intramammary infections with pathogens entering the mammary gland through the teat canal.

  • Based on the occurrence or nonoccurence of clinical signs, mastitis can be differentiated into clinical and subclinical mastitis.

  • Clinical mastitis is characterized by alterations in the milk and by inflammation of the affected quarter, with or without systemic clinical signs.

  • The most important tool to monitor subclinical mastitis is testing milk for SCCs and the calculation of key performance indicators; treatment may or may not be indicated.

  • Antimicrobial treatment of clinical mastitis should be based on the identification of the causative pathogen. Severely affected cows may also require fluids, electrolytes, and anti-inflammatory drugs.

  • Mastitis prevention strategies include pre- and postmilking antiseptic teat dip, a hygienic milking routine, and dry, adequate bedding.

For More Information


  1. Gorden PJ, Kleinhenz MD, Ydstie JA, et al. Efficacy of vaccination with a Klebsiella pneumoniae siderophore receptor protein vaccine for reduction of Klebsiella mastitis in lactating cattle. J Dairy Sci. 2018;101(11):10398-10408. doi:10.3168/jds.2017-14267

  2. Green MJ, Green LE, Cripps PJ. Comparison of fluid and flunixin meglumine therapy in combination and individually in the treatment of toxic mastitisVet Rec. 1997;140(6):149-152. doi:10.1136/vr.140.6.149

  3. Lohuis JA, Van Leeuwen W, Verheijden JH, Brand A, Van Miert AS. Flunixin meglumine and flurbiprofen in cows with experimental Escherichia coli mastitisVet Rec. 1989;124(12):305-308. 

  4. Anderson KL, Smith AR, Shanks RD, Davis LE, Gustafsson BK. Efficacy of flunixin meglumine for the treatment of endotoxin-induced bovine mastitisAm J Vet Res. 1986;47(6):1366-1372.

Test your Knowledge nowTake a Quiz!
Download the free Merck Vet Manual App iOS ANDROID
Download the free Merck Vet Manual App iOS ANDROID
Download the free Merck Vet Manual App iOS ANDROID