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Mastitis in Cows

Signs, causes, treatment and prevention

Mastitis is one of the most prevalent and costly diseases of dairy cows worldwide. The estimated annual cost to the US dairy industry alone is US$2 billion. The causes and management of bovine mastitis are complex, but various measures can be implemented to optimize udder health and productivity in dairy herds.

Definition of mastitis

Mastitis is an inflammation of the mammary gland generally associated with intramammary infection (IMI). Bacteria are the most common etiological agent, but other microbes such as fungal species (yeasts or molds), certain microscopic algae (Prototheca spp.), and viruses can cause IMI. Physical trauma or chemical irritation are less common causes of mastitis.

A link between mastitis and endotoxins in high producing dairy cows? Remarks from James Cullor of the School of Veterinary Medicine, University of California – Davis (USA) at the 2016 World Nutrition Forum

Mastitis costs 

Economic losses stem from reduced milk production and decreased milk quality.  Farmers must discard milk from cows with clinical cases of mastitis and from cows undergoing antibiotic treatment according to withdrawal periods in order to provide time for antibiotics to clear the cow’s body.

Mastitis also alters the composition and properties of milk, resulting in reduced cheese yields and shortened shelf life of manufactured dairy products. Treatment and veterinary costs rise, as do labor costs, and milking parlor efficiency can decrease due to increased time spent attending to mastitic animals.

In addition to economic losses, animal welfare is a concern as studies have shown that mastitis can be painful and cause discomfort to cows. Thus, cows diagnosed with clinical mastitis, or those with persistent subclinical mastitis have a greater risk of being culled. 

Indeed, udder health issues are frequently cited as one of the top three reasons for culling of dairy cows. Low milk production, potentially associated with mastitis, is another leading cause of culling in dairy herds. Toxic mastitis, an acute form of the disease resulting in severe inflammation and septicemia, can even lead to cow death. 


Mastitis categories  

There are multiple ways to classify cases of mastitis. 

The first major classification has to do with the origin of the pathogen: contagious vs. environmental (Table 1). A broad spectrum of bacteria have been isolated from infected mammary gland secretions, but a relatively small array of species are frequently detected. 

Contagious pathogens are spread cow-to-cow, typically during milking as infected mammary glands serve as the primary reservoir for such microbes. Contagious pathogens include Staphylococcus aureus, Streptococcus agalactiae, and Mycoplasma spp. 

Environmental pathogens are those which primarily reside in the cow’s normal habitat. Cows are primarily exposed to these pathogens between milkings when teat ends come in contact with contaminated bedding, manure, contaminated water, or soil. Common environmental pathogens include Escherichia coli, Klebsiella spp., and environmental streptococci such as S. uberis and S. dysgalactiae. There are many other microorganisms that have been isolated from cases of mastitis and are associated with the cow’s environment.

Coagulase negative staphylococci (CNS) are normal flora of the skin and these organisms can act as opportunistic pathogens when they enter the mammary gland. A hot topic in the world of mastitis research revolves around differentiating CNS to better understand the differences in their effects on milk quality and yield. 

Table 1. Contagious and environmental mastitis | Source: BIOMIN

 Contagious mastitisEnvironmental mastitis
ReservoirInfected mammary glandsThe cow’s environment, including: 
  • Bedding/stalls/soil
  • Manure
  • Water
Exposure Spread from cow-to-cow, including via:
  • Milking equipment
  • Milkers’ hands or towels
  • Flies and other vectors
Constant exposure exacerbated by heat and humidity

The distinction of acute vs. chronic mastitis has to do with the timing and duration of the disease (Table 2). 

Table 2. Signs of acute and chronic mastitis | Source: BIOMIN

Acute mastitisChronic mastitis
Sudden onset, but often quickly resolvedContinues over a long period of time
Swelling, heat, discoloration, hardening of the glandOften subclinical
PainPotentially painful
Grossly abnormal milk‘Flare-ups’ or periodic acute events
Noticeable decrease in milk yieldLess obvious decrease in milk yield

Differentiation of clinical vs. subclinical mastitis is determined by the presentation of the disease. Clinical cases are relatively easy to identify due to the presence of visual changes or abnormalities of the milk and/or mammary gland. 

Clinical cases may present with any of the following signs: 

  • Flakes or clots to purulent exudate 
  • Discolored, watery, or bloody milk 
  • Swelling or hardening of the gland
  • The presence of pain, heat or reddish discoloration of the skin of inflamed glands

Systemic signs of illness may also occur, including: 

  • Increased rectal temperature 
  • Anorexia
  • Decreased reticulorumen motility
  • Lethargy 
  • Potentially death 

Severity of clinical mastitis cases can range from mild to severe. The clinical rating depends of the range and severity of the signs observed. 

In contrast, subclinical mastitis cases often go unrecognized, as the milk and gland appear normal. Although subclinical mastitis is more difficult to identify, monitoring of somatic cell count (SCC) or bacteriological culturing of milk can detect the presence of inflammation or IMI. 

The different mastitis classifications are not mutually exclusive. For instance, a cow could have an acute clinical case of environmental mastitis.

Predisposing factors

As a multifactorial disease, mastitis has many causes and predisposing factors which are outlined in Table 3.

Milking parlor management including milking routine best practices are essential to limiting mastitis risk in a herd. The milking system must be well maintained to ensure that properly functioning, clean equipment is used to harvest milk. Relatively few IMI are attributed to correctly functioning milking machines; however, improperly functioning milking equipment can result in a high rate of new IMI. Proper milk line vacuum and duration of milking must be optimized as over-milking can damage the teat end, increasing the likelihood of mastitis. Insufficient milk removal can also predispose cows to mastitis and decrease overall milk production. 

Since the environment plays a large role in mammary health, good hygiene in the parlor as well as in the barn are essential to reducing mastitis risk. Clean sand bedding is considered the gold standard, as inorganic material does not support the growth of pathogens. The greater the organic content of the sand, the less protective it will be. 

Factors beyond control, including the weather, also increase the risk of mastitis. Increased temperatures and humidity better support pathogen growth in the cow’s environment as well as increase stress in the cow, reducing her resistance to infection.

There are anatomical, cellular, and soluble defense mechanisms that help protect the mammary gland from infection. Pathogens must gain entry into the mammary gland via the teat canal in order to cause IMI. The first line of defense against IMI is the innate immune system. Anatomical features of the teat serve as physical barriers that help prevent establishment of infection. The teat sphincter muscles keep the teat opening closed between milkings. Post-milking, the teat sphincter muscles can take at least 2 h to close the teat opening, so this period is crucial for mammary defense. Additionally, the teat canal is lined with a waxy substance called keratin that has antimicrobial properties to help impede pathogen infiltration into the gland.

Coordinating the delivery of fresh feed while cows are in the parlor will entice cows to eat and remain standing upon return to the pen. This provides time for the teat sphincters to close and limits pathogens from entering the teats following milking.

Nutrition can also play a role in mastitis risk. Cows in negative energy balance, especially transition cows, are more susceptible to infection. Diets must also meet vitamin and mineral requirements for proper immune function. 

Surfaces and alleys moving into the parlor as well as the holding pen must provide firm footing and cow flow should be smooth (a combination of good design and stress free handling), thus reducing the risk of physical injury to teats. Damage to teat end tissue facilitates bacterial entry into the gland.

Table 3. Predisposing factors of mastitis | Source: BIOMIN

Improperly working milking equipment
Teat end damage

  • Resistance
  • Mammary structure
  • Age


  • Milking routine including pre- and post-dip application 
  • Hygiene – milking parlor and barn 
  • Bedding 
  • Nutrition 
  • Vaccination program 
  • Dry cow therapy 
  • Transition cow management 
  • Heifer management 
  • Immune suppression 
  • Transition period 
  • Mycotoxins



Mycotoxins can suppress the immune system of animals. Cows experience a great deal of stress around parturition due to the many physiological changes that occur with calving and the onset of lactation. Mycotoxins in cattle feed can exacerbate this stress via immune dysfunction and decreased feed intake, deepening negative energy balance and increasing the risk of metabolic disorders and infectious diseases. Deoxynivalenol (DON) and other trichothecenes can disrupt protein synthesis, which can reduce white blood cell populations and cellular functions as well as limit production of important inflammatory mediators. In addition, some of the ergot alkaloids and trichothecenes can cause dermal lesions and gangrenous necrosis that disrupt the integrity of the teat and teat skin, potentially contributing to an increased risk of mastitis.  

Table 4 highlights some of the main consequences of mycotoxins in dairy cows in relation to mammary health and milk production. Reduced milk production results from several factors, including a decrease in intake or feed refusal that is commonly reported with certain mycotoxins such as DON. Mycotoxins can alter rumen function by changing the microbial populations or the breakdown of nutrients, consequently reducing nutrient absorption and impairing metabolism which ultimately leads to reduced availability of the precursors needed for milk synthesis.

Table 4. Potential mammary-related negative effects of mycotoxins in dairy cows | Source: BIOMIN

1. Reduced milk production
2. Toxic contaminants in milk, especially Aflatoxin M1
3. Increased risk of mastitis
4. Altered milk composition

Reduced milk quality

Reduced milk quality stems primarily from increased SCC. Somatic cells, specifically neutrophils, increase in number in the mammary gland during mastitis to combat invading pathogens. Mycotoxins can reduce neutrophil function, making the cow’s immune response less effective, which in turn increases the severity and duration of infection. 

Additionally, mastitis causes alterations in the concentration of milk components including changes in fat, protein, lactose, and mineral content. Compared with milk from healthy cows, that of affected cows can show mineral changes that include increased sodium and reduced potassium levels.

These differences negatively impact the manufacturing quality of milk. Milk processors want to obtain the highest quality milk to improve the yield and shelf life of manufactured products such as cheese. 



Since milking equipment can serve as a fomite (inanimate object that can transfer infection), proper hygiene is essential.  

The use of post-milking disinfectant teat dip and antibiotic dry cow therapy (DCT) has helped reduce the prevalence of contagious mastitis. Environmental pathogens are less likely to be spread during milking, but use of germicidal pre-milking teat dip prior to milking can reduce this risk. 

The dry period is critical for good udder health and optimal productivity in the following lactation. Use of antimicrobial DCT provides an opportunity to eliminate existing IMI and provides protection against new IMI during the early dry period. This period of non-lactation gives producers an opportunity to treat existing IMI without losses associated with discarded milk due to antimicrobial treatment; however, the periods immediately following dry-off and before calving are associated with an increased susceptibility to new IMI

Various management practices have helped with prevention of mastitis in cows caused by contagious pathogens, but have not proven to limit environmental infections. Well-managed herds have been successful in limiting contagious IMI; however, environmental mastitis has continued to be a challenge since even the cleanest stalls and surroundings can harbor microorganisms. Control of contagious IMI is possible and repeatable across herds when implementing best practices. The fight against mastitis has refocused on limiting the prevalence of environmental IMI. 

incidence of new intramammary infection during the lactation cycle.
A schematic illustration of the incidence of new intramammary infection (IMI) during the lactation cycle. The greatest rates of new IMI occur around the time of calving and again after drying off.
Source: Bradley and Green, 2004


Vaccines have been designed to combat mastitis, but many are of limited protection against coliform infections. Studies have shown that the J5 core antigen vaccine is efficacious in reducing the incidence of clinical mastitis caused by E. coli, especially during early lactation, but did not reduce the prevalence of infection. Vaccines can be valuable in reducing the duration and severity of IMI. The benefits of use of the J5 vaccine have been proven worthwhile since the mid-1990s. 


Mycotoxins should be considered as a potential factor that may negatively affect udder health and productivity. Mycotoxin risk management includes detection, prevention, and mitigation. Screening feeds for the presence of mycotoxins can help identify contamination and limit exposure through ration adjustments including inclusion rate modifications and potential ingredient changes. Implementation of an in-feed mycotoxin counteracting product should also be considered. Clay mineral binders are not effective against all mycotoxins, therefore a combination approach including biotransformation components that can degrade mycotoxins that are not readily controlled through binding as well as bioprotection components which support liver health, immune function, and gut integrity will provide broad-spectrum protection. 


Bannerman, D.D., A.C.W. Kauf, M.J. Paape, H.R. Springer, and J.P. Goff. 2008.  Comparison of Holstein and Jersey innate immune responses to Escherichia coli  intramammary infection. J. Dairy Sci. 91:2225-2235. 

Burvenich, C., V. van Merris, J. Mehrzad, A. Diez-Fraile, and L. Duchateau. 2003. Severity of E. coli mastitis is mainly determined by cow factors. Vet. Res. 34:521-564. 

Bradley, A.J., and M.J. Green. 2004. The importance of the nonlactating period in the epidemiology of intramammary infection and strategies for prevention. Vet. Clin. Food Anim. 20: 547-568. 

Harmon, R.J. 1994. Physiology of mastitis and factors affecting somatic cell counts. J. Dairy Sci. 77:2103-2112. 

Hogan, J.S. and K.L. Smith. 2003. Coliform mastitis. Vet. Res. 34:507-519. 

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

Hogan, J.S., K.L. Smith, D.A. Todhunter, and P.S. Schoenberger. 1992a. Field trial to determine the efficacy of an Escherichia coli J5 mastitis vaccine. J. Dairy Sci. 75:78-84. 

Hogan, J.S., W.P. Weiss, D.A. Todhunter, K.L. Smith, and P.S. Schoenberger. 1992b. Efficacy of an Escherichia coli J5 mastitis vaccine in an experimental challenge. J.  Dairy Sci. 75:415-422. 

Hogan, J.S., W.P. Weiss, K.L. Smith, D.A. Todhunter, P.S. Schoenberger, and L.M.  Sordillo. 1995. Effects of an Escherichia coli J5 vaccine on mild clinical coliform mastitis. J. Dairy Sci. 78:285-290. 

Leslie, K. E. and C. S. Petersson-Wolfe. 2012. Assessment and management of pain in dairy cows with clinical mastitis. Vet. Clin. North Am. Food Anim. Pract. 28:289-305. http://dx/doi.org/10.1016/j.cvfa.2012.04.002. 

National Mastitis Council. 2016. Current Concepts of Bovine Mastitis, 5th ed. The National Mastitis Council, Inc. 

National Mastitis Council. 1999. Laboratory Handbook on Bovine Mastitis-Revised Edition. The National Mastitis Council, Inc. 

NMC. 2004. Microbial Procedures for the Diagnosis of Bovine Udder Infection and Determination of Milk Quality. The National Mastitis Council,  Inc. 

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

Sordillo, L.M. and K.L. Streicher. 2002. Mammary gland immunity and mastitis susceptibility. J. Mammary Gland Bio. And Neoplasia. 7:135-146. 

Wellenberg, G.J., W.H.M. van der Poel, and J.T. van Oirschot. 2002. Viral infections and  bovine mastitis: a review. Veterinary Microbiology. 88:27-45. 

Zhao, X., and P. Lacasse. 2008. Mammary tissue damage during bovine mastitis: causes  and control. J. Anim. Sci. 86(Suppl. 1):57-65.