ISSN 2398-2993      

Mastitis: staphylococcus aureus


Tom Greenham

Peter Down

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  • Cause: infection of the mammary tissue with Staphylococcus aureus bacteria (S. aureus).
  • Signs: clinically, inflammation of the affected mammary gland, altered visual appearance of the milk and reduced milk production may be observed. Sub-clinical presentations are common, with increased somatic cell count in the absence of visible signs.
  • Diagnosis: bacterial culture of milk from quarters of the udder where clinical signs have been detected. Other diagnostic tools are available, for example milk polymerase chain reaction (PCR) tests, as discussed in more detail.
  • Treatment: intramammary and systemic antibiotics have been combined with various local and systemic anti-inflammatory preparations in many varied protocols.
  • Prognosis: a clinical cure may be readily affected, but a bacterial cure is less frequently achieved, leading to persistent infection, with recurrence of the clinical and sub-clinical presentations being common.



  • S. aureus Staphylococcus spp is one of many etiological agents for clinical and sub-clinical mastitis.
  • The S. aureus bacterium is often described by the result of various bacteriological tests, being referred to as a Gram-positive and coagulase-positive coccus.
  • Numerous strains of S. aureus have been isolated, from a wide number of animal species. Specificity to the original host is low, with strains readily being transmitted across species, including between humans and other mammals.
  • Different strains have a moderate degree of genetic variation, resulting in a range of virulence factors.
  • Virulence factors include:
    • The ability to hydrolyse casein and ferment lactose, making milk an ideal growth medium.
    • Bacterial wall surface adaptations that enhance the ability to adhere to epithelial cells and colonize the teat canal.
    • Antiphagocytic properties which allow evasion of the neutrophil response in the udder.
    • An ability to survive inside macrophages and mammary cells.
  • The origin of the S. aureus pathogen is the skin surface of cows within the herd. Not all strains of S. aureus isolated from the skin are associated with intramammary infection, but the skin sites of the udder, teats and hocks are particular reservoirs of mastitis-associated strains.
  • Survival times of S. aureus in the environment tend to be low, although there is a positive relationship between the number of bacteria present and the duration to negative culture result. Some researchers have demonstrated survival times ranging from one to fifty-six days for S. aureus on surfaces such as cotton and plastic. This indicates a significant role of fomites in the transmission of S. aureus between cows Pathogen transmission: overview.

Predisposing factors

  • S. aureus intramammary infection requires two key events to occur:
    • The entry of the bacteria in to the teat.
    • Evasion of the host’s immune response.
  • These events can be facilitated by several key predisposing factors.
    • Compromised integrity of the anatomy of the teat sphincter is associated with increased intramammary infection, presumably as a result of an increased likelihood of bacterial invasion of the teat.
    • In addition to exerting an effect on teat end integrity, the milking machine may also be directly responsible for transferring S. aureus bacteria across the teat sphincter.
    • Under certain conditions, detachment of the milking unit can generate a vacuum gradient that reverses the direction of flow through the teat. This has the potential to cause injection of milk, air and pathogens up in to the teat from the teat end. The significance of these events in generating intramammary infections is not yet fully established .
    • The introduction of S. aureus bacteria to teat sinus and mammary tissue does not automatically result in an established infection. The mammary immune defences, particularly the recruitment of polymorphonuclear neutrophils, can successfully eliminate the bacterial population resulting in self cure. However, it has been demonstrated that if only low numbers of neutrophils are recruited, or if the function of the neutrophils is impaired, S. aureus infection is more likely to occur. As such any physiological or pathological process that impairs immune function may predispose intramammary infection with Staphylococcus aureus.


  • For S. aureus to establish an intramammary infection, firstly it must be present at the teat orifice.
    • This teat end contamination does not have to be extensive, as an intramammary infection may be established from as little as ten colony forming units of S. aureus.
  • S. aureus bacteria may inhabit the teat end naturally or may be transferred there from other sources.
    • Hock skin often contacts the teat when the cow is recumbent, and this may result in transfer of bacteria between these sites.
    • Udder skin may harbor S. aureus with gravity aiding the transfer from udder to teat, particularly if the udder skin is wet.
    • Other common methods of teat end contamination include the hands of milking staff passing from cow to cow, or the liners of the milking machine being used on consecutive animals without disinfection
  • Once present at the teat orifice the S. aureus bacteria must traverse the teat sphincter to enter the teat canal.
    • These bacteria are not motile and so require environmental factors to aid this transport.
    • This process is incompletely understood, but there is a growing body of evidence to implicate certain conditions of machine milking as having a role in transfer of pathogens across the teat sphincter.
  • On entering the teat canal S. aureus bacteria adhere to the epithelial cells, colonising the teat canal. It is thought that the closer this adherence is to the teat sinus the greater the risk of intramammary infection.
  • From the teat canal, S. aureus bacteria enter the gland cistern, either by progressive colonisation or, as some researchers have proposed, by altered intramammary pressure dynamics when the animal walks, lies down or is milked. Within the glandular tissue, the bacteria adhere to mammary epithelial cells, thought to facilitate the establishment of infection, and also adhere to fat globules, thought to allow dissemination throughout the quarter of the udder.
  • S. aureus bacteria are able to invade mammary epithelial cells, leading to erosion and ulceration of the lactiferous sinus and ducts as well as lesions of the alveolar secretory cells.
  • Occlusion of the alveolar ducts allows localized populations of S. aureus to evade both intramammary antimicrobial treatments and host leukocytes, surviving to propagate the infection on release from the occluded alveolus.
  • These focal regions of trapped bacteria may progress to form microscopic abscesses or granulomas.
  • S. aureus also causes tissue damage remote to the location of the bacteria, by secretion of toxins and enzymes in to the mammary gland.


  • A period of 3 to 6 days is commonly seen between invasion of the teat and establishment of an infective population within the mammary tissue.
    • After this period clinical mastitis may be observed, but in the case of subclinical infection the lag time between initial infection and detection may be much longer.
  • Left untreated, or with poor response to treatment, a S. aureus intramammary infection will often become chronic, persisting for numerous months -sometimes for the remainder of the animal’s lactation Mastitis: approach to the cow with chronic mastitis.


  • S. aureus is described as a ‘contagious’ mastitis pathogen, with infection following transmission between cows, invariably through fomites associated with the milking process such as the liner of the milking machine; teat-preparation materials that are shared between cows such as dip-cups or teat brushes; and the hands of the milking team Pathogen transmission: overview.
  • Transmission within the herd can be described by the infection ‘reproduction number’ -that is the number of new cases that each S. aureus intramammary infection will generate during its duration. This number can be affected by factors such as the general level of herd immunity, or the teat end condition within the herd. Poor herd level immunity (or a high proportion of rough teat ends) will increase the reproduction number and lead to a higher number of new infections within the population.
  • This contagious ‘reproduction’ of infection gives a relatively consistent epidemiological picture between S. aureus positive herds.
  • Incidence of clinical mastitis is usually moderate, although poor cure rates lead to a moderate to high prevalence.
  • Prevalence of intramammary infection is dictated by new infection rate, duration of persistence and elimination rate. New infection rate is itself affected by prevalence, with a positive association between herd prevalence and odds of new infection.
  • Data for both clinical and subclinical infection will show no evidence of seasonality and no strong association with stage of lactation. Case distribution is that of ‘lactational’ origin rather than ‘dry period’ origin. It may appear as if there is a high incidence of early lactation cases, but many of these are uncured infections from the previous lactation.
  • A key indicator of a significant S. aureus presence in the population is the cure rate over the dry period. Of the cows that start their dry period with a cell count above 200,000/ml, more than eighty per cent would be expected to enter the next lactation with a cell count less than 200,000/ml. If this benchmark is not achieved a persistent pathogen such as S. aureus may be suspected, particularly if there is no evidence of a high incidence of intramammary infections of dry period origin.
  • The notable feature of S. aureus infection at a herd level is an ongoing increase in the proportion of the milking herd with chronically high somatic cell counts Somatic cell count:
    • This will be highlighted by individual cow milk recording data, but may or may not be reflected in the bulk milk cell count, depending on the herd’s policy of discarding milk from animals with high cell count.
    • Cows can be classed as ‘chronically’ infected if they have two consecutive months with somatic cell counts over 200,000/ml.
    • For primiparous animals a threshold of 150,000 cells/ml may be appropriate.
      • This is partly due to a naturally lower level of cells in the milk, but also due to the importance of maximising test sensitivity in primiparous animals to allow reduction of culling and yield loss in the first lactation.
    • These parameters are chosen to reflect the likelihood of infection of an individual quarter when using a composite cell count of all four quarters.
    • Higher or lower thresholds can be used to improve this assumption’s specificity and sensitivity respectively.


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Further Reading


Refereed Papers

  • Recent references from PubMed and VetMedResource.
  • Dulon M, Haamann F, Peters C, Schablon A & Nienhaus A (2011) MRSA prevalence in European healthcare settings: a review. BMC Infectious Diseases 11, 138-151 PubMed.
  • Capurro A, Aspán A, Ericsson Unnerstad H, Persson Waller K & Artursson K (2010) Identification of potential sources of Staphylococcus aureus in herds with mastitis problems. J Dairy Sci 93, 180–191 PubMed.
  • Barkema H W, Schukken Y H & Zadoks R N (2006) Invited Review: The Role of Cow, Pathogen, and Treatment Regimen in the Therapeutic Success of Bovine Staphylococcus aureus Mastitis. J  Dairy Sci 89, 1877–1895 PubMed.
  • Cucarella C, Tormo M A, Ubeda C, Trotonda M P, Monzon M, Peris C, Amorena B, Lasa I & Penades J R (2004) Role of biofilm-associated protein bap in the pathogenesis of bovine Staphylococcus aureus. Infect Immun 72, 2177–2185 PubMed.
  • de Haas Y, Barkema H W & Veerkamp R F (2002) The Effect of Pathogen-Specific Clinical Mastitis on the Lactation Curve for Somatic Cell Count. J Dairy Sci 85, 1314–1323.
  • Deluyker H A, Chester S T & VanOye S N (1999) A multilocation clinical trial in lactating dairy cows affected with clinical mastitis to compare the efficacy of treatment with intramammary infusions of a lincomycin/neomycin combination with an ampicillin/cloxacillin combination. J Vet Pharmacol Ther 22, 274–282 PubMed.
  • Anderson J C (1976) Mechanisms of Staphylococcal Virulence in Relation to Bovine Mastitis. British Veterinary Journal 132 (3), 229-245.

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