• Peracute: swelling, pain, heat and abnormal secretion in the mammary gland are accompanied by signs of systemic disturbance such as fever, depression, anorexia, weakness and a rapid, weak pulse. The signs are those of a toxaemia or septicaemia. Gangrenous mastitis is included in this category.

• Acute: changes in the mammary gland are similar to those of peracute mastitis but the systemic signs are much less severe.

• Subacute: no systemic reaction and the changes in the gland are less marked.

• Chronic: there are no systemic signs and very few external signs of change in the udder, but abnormal secretion in the gland occurs intermittently.

• Subclinical: the infection in the mammary gland is detectable only by bacterial culture or by tests to demonstrate a high leukocyte count in the milk. There is no obvious change in the appearance of the milk. Staphylococcus aureus is notorious for causing a high percentage (up to 50% of the herd) of subclinical infections in dairy herds with a staphylococcal mastitis problem.

Staphylococcal mastitis

Affected quarters often have large numbers of Staphylococcus aureus in the milk. The staphylococci are easily transmitted during milking via the teat cups or milkers’ hands. Following entry to the mammary gland, adhesins such as fibrinogen-binding protein and fibronectin-binding protein A are likely to be important in adherence to mammary epithelial cells (Castagliuolo et al. 2006). Staphylococcus aureus strains with enhanced ability to survive within both phagocytes and mammary epithelial cells are more likely to set up infection and to persist in the face of the host immune response and antimicrobial therapy. Biofilm formation is now considered to be a factor in persistent infections also (Melchior et al. 2006). The type of mastitis produced by S. aureus ranges from subclinical to the peracute life-threatening forms, one of which is gangrenous mastitis. Gangrenous mastitis is caused by the action of alpha toxin (alpha haemolysin) that damages blood vessels, resulting in ischaemic coagulative necrosis of adjacent tissue. The affected quarter becomes purplish and cold and will eventually slough, if the animal survives the toxaemia. However, subclinical and chronic forms of mastitis are the most common and economically significant types of S. aureus mastitis worldwide. Both lead to a gradual replacement of secretory tissue with fibrous tissue and a subsequent loss of milk production by the affected quarter. The chronic and subclinical forms of mastitis respond poorly to antimicrobial therapy, the reasons for which include host, pathogen and treatment factors (Barkema et al. 2006). Host factors such as age of cow, cell count and duration of infection influence treatment outcome as does treatment duration. Pathogen factors affecting cure rates include the ability to survive intracellularly, biofilm formation and antimicrobial resistance. Apart from therapeutic considerations, the emergence of MRSA as a cause of mastitis is of public health concern, in particular the emergence of a divergent mecA gene in bovine clones of S. aureus and the possibility that cattle may serve as a source for the emergence of new MRSA strains in humans (Garcia-Alvarez et al. 2011, Shore et al. 2011).

Streptococcus agalactiae

Although no longer a common cause of mastitis in major dairying areas, Streptococcus agalactiae, may be a significant problem in individual herds. It is an obligate parasite of the bovine mammary gland. The organism can adhere to mammary epithelial cells but does not invade the interstitial tissue. Few data on specific virulence factors of mastitis-producing strains of S. agalactiae have been published and most information relates to human strains. The production of a capsule allowing protection against phagocytosis is likely to be of importance. Streptococcus agalactiae secretes a number of enzymes and haemolysins which have a probable role in destruction of mammary tissue. Following establishment of infection, there is rapid multiplication of the bacterium with a great outpouring of neutrophils into the ducts and damage to the ductal and acinar epithelium. Ducts are obstructed with cells and debris causing involution of the acini in the affected lobules. Fibrosis of interalveolar tissue occurs, resulting in a loss of secretory function.

Mycoplasmal mastitis

Although mycoplasmal mastitis can be clinically severe, there is rarely any systemic involvement. Mycoplasma bovis is the most important species involved and is particularly important in very large dairy herds. Cows of all ages and all stages of lactation can be affected, with those that have recently calved showing the most severe signs. There can be long-term persistence of the organisms in udders and subclinically affected animals are an important source of infection. Haematogenous spread between quarters occurs. The role of the known virulence factors of M. bovis in the pathogenesis of mastitis is not entirely clear. Surface proteins are likely to have a role in adherence and immune evasion in the mammary gland as has been shown for other host tissues. The secretion from an affected quarter appears fairly normal in the early stages of infection, but if the milk is allowed to stand, a deposit of fine, flaky material settles out leaving a turbid, whey-like supernatant fluid. Leukocyte counts in the milk are usually very high, often over 20 million cells/mL.

Coliform mastitis

Up to 65% of cases of E. coli mastitis occurring during the first two months of lactation are the result of infection acquired during the dry period (Smith et al. 1985). It is thought that the survival and multiplication of E.coli strains within the dry mammary gland is dependent in part on the ability of the pathogen to acquire iron (Hogan & Smith 2003). Escherichia coli and other coliforms can multiply rapidly in quarters with a low cell count. The immune response of the host is a major determinant of the outcome of infection and both the somatic cell count and the speed of recruitment of neutrophils into the mammary gland affect the course and severity of the mastitis episode (Shuster et al. 1996). The inflammatory reaction destroys a large proportion of the bacterial population. When Gram-negative bacteria die and lyse, endotoxin is released from the cell wall. The sudden liberation of endotoxin can result in a severe toxaemia that is life-threatening. Approximately 10% of clinical coliform cases result in severe systemic signs (Hogan & Smith 2003). Unlike infections with contagious pathogens, coliform mastitis tends to be of short duration with E. coli infections during lactation typically lasting less than 10 days (Todhunter et al. 1991). However, there is evidence that this pattern may be changing and persistent infections with E. coli may be becoming more frequent (Bradley & Green 2001).

Streptococcus uberis

This organism is a commensal of the tonsils, gastrointestinal and genital tract of cattle and is found on the coat and in the environment. Faecally contaminated bedding is an important source of infection but heavily used pasture may carry high levels of the pathogen also. The organism is classified as an environmental pathogen but a specific molecule involved in adherence to bovine mammary epithelial cells has been demonstrated (Almeida et al. 2006). Streptococcus uberis produces exoenzymes including a plasminogen activator which converts plasminogen to plasmin. Plasmin is a protease which in turn can hydrolyse casein to peptides which the organism then uses for growth. Production of a capsule confers resistance to phagocytosis. Only a few infections result in systemic signs of fever and inappetance, with clinical signs usually limited to abnormalities in the milk.

Streptococcus dysgalactiae

Streptococcus dysgalactiae has been classified as both a contagious and environmental pathogen. It is found in the environment of cows as well as colonizing the tonsils and mucosa of the mouth and genital tract. It is able to persist within the mammary gland although the mechanism whereby it survives within mammary epithelial cells is unknown. It is isolated relatively infrequently from clinical and subclinical cases of mastitis, 1.5% and 0.4% respectively in a survey by Bradley et al. (2007), but is associated with ‘summer mastitis’ also.