Mastitis

What it is

Mastitis is inflammation of one or more quarters of the udder. It is almost always caused by an intramammary infection with bacteria that pass through the teat canal. The inflammatory response brings large numbers of neutrophils into the milk, which together with epithelial cells make up the somatic cells; their count is the main measure of udder health.

• Clinical mastitis: there are visible changes. It is graded as mild (abnormal milk only: clots, watery or serous appearance), moderate (also a swollen, hot or painful quarter) and severe (also systemic signs).
• Subclinical mastitis: the milk and the quarter look normal, but the somatic cell count (SCC) rises and yield falls. It is far more common than clinical mastitis.

Pathogens are grouped by their origin:

• Contagious: they live in the udder and spread from cow to cow during milking (hands, liners, cloths). The main ones are Staphylococcus aureus, Streptococcus agalactiae and Mycoplasma bovis. They tend to cause persistent subclinical infections.
• Environmental: they come from bedding, manure and the surroundings, and enter between milkings or during the dry period. The most important are coliforms (Escherichia coli, Klebsiella) and Streptococcus uberis. They usually cause short clinical cases; some coliforms cause severe mastitis with endotoxaemia.

Who it affects

Mainly dairy cows, although any female bovine can be affected. The risk of new infections is highest at the start of the dry period and around calving, and clinical mastitis is most common in early lactation. Risk is increased by the number of lactations, teat injuries and teat-end hyperkeratosis, poor milking routines or milking machines, dirty or wet bedding, hypocalcaemia and other postpartum diseases.

Anatomy involved

• Teat canal: the entry point for almost all infections. Its keratin lining and the teat sphincter form the main barrier; after milking the sphincter is slow to close, and during that interval bacteria enter more easily. Severe hyperkeratosis of the teat end, caused mainly by machine milking, weakens that barrier.
• Cisterns and ducts: bacteria ascend from the teat cistern to the gland cistern and the lactiferous ducts.
• Secretory tissue (alveoli): where the damage occurs. Chronic infections, especially with S. aureus, form microabscesses and fibrosis that wall off the bacteria and hinder cure.
• Independent quarters: each quarter has its own duct system, so infection usually stays confined to one quarter and milk is tested per quarter.
• Mammary lymph nodes: at the caudal base of the udder; they may enlarge in mastitis.

Clinical signs

• Abnormal milk: clots, flakes, watery or serous appearance, blood or pus.
• Affected quarter: swollen, hot, painful and firm or hard.
• Severe mastitis: fever (or low temperature in endotoxic shock), anorexia, depression, ruminal stasis, dehydration, diarrhoea and recumbency; typical of coliform infections.
• Gangrenous mastitis: a cold, bluish to black quarter that eventually sloughs; associated mainly with S. aureus.
• Chronic mastitis: repeated clinical episodes or a persistently high SCC, with fibrotic quarters and lower yield.
• Subclinical mastitis: no signs; detected only by SCC or culture.

Diagnosis

• Forestripping: examining the first streams of milk from each quarter before milking, on a dark surface, to detect abnormal milk.
• California Mastitis Test: a cow-side test that estimates the somatic cells in each quarter.
• Somatic cell count: the monthly individual SCC from milk recording identifies cows with probable subclinical infection (the most widely used threshold is 200,000 cells/mL); bulk tank SCC reflects the herd situation and is subject to legal limits.
• Bacteriological culture of aseptically collected milk, in the laboratory or on the farm, and PCR: they identify the pathogen, help distinguish contagious from environmental problems and guide treatment. A single culture can miss the infection.

Treatment and prevention

• Mild or moderate mastitis: intramammary antimicrobials, chosen according to the pathogen when it is known. Many cases caused by Gram-negative bacteria or with no bacterial growth cure without antibiotics, so culture-guided treatment reduces their use.
• Severe mastitis: an emergency. Fluid therapy, non-steroidal anti-inflammatory drugs, frequent stripping of the quarter and, depending on the case, systemic antimicrobials.
• Cows with chronic S. aureus infection that do not respond: drying off the quarter or culling the cow, because cure is unlikely and they are a source of infection.
• Prevention:
  • A good milking routine: teat preparation and drying, gloves and post-milking teat disinfection.
  • Milking machine maintenance to protect the teat end.
  • Clean, dry bedding.
  • Dry cow therapy, with antimicrobials in all cows or only in infected ones (selective therapy), and internal teat sealants.
  • Prompt treatment of clinical cases and culling of chronically infected cows.
  • Monitoring of individual and bulk tank SCC, and segregation or milking last of cows infected with contagious pathogens.

Drug use in food-producing animals is subject to each country's regulations and to withdrawal periods for milk and meat; milk from treated cows cannot be used for human consumption during that period.

Key studies

• Pantoja et al. (2020), systematic review of 18 studies (8 prospective cohorts, 9 cross-sectional and 1 case-control) on teat-end hyperkeratosis. Severe hyperkeratosis was a risk factor for clinical and subclinical mastitis, especially with S. aureus, while mild hyperkeratosis was not and might even be protective. The most common limitation of the studies was failure to control for confounding.
• Dohoo et al. (2011), evaluation of criteria for diagnosing intramammary infection from a single culture, using 25,886 sets of three samples and another 784 quarters sampled three times as the reference. Except for S. aureus, the sensitivity of every criterion was below 90% (and in many cases below 50%), while specificity was high for most species. A negative culture does not rule out infection.
• Lago et al. (2011), randomised trial in 422 cows (449 quarters) with mild or moderate mastitis from 8 herds in the United States and Canada. With on-farm culture-guided treatment, 51% of cases received intramammary antibiotics compared with 100% in the control group. There were no significant differences in days to clinical cure (3.2 vs 2.7), bacteriological cure (60% vs 71%), new infections (50% in both) or treatment failure (78% vs 81%).
• Nobrega et al. (2020), systematic review and network meta-analysis of 30 studies on non-severe clinical mastitis. Antimicrobials of critical importance for human medicine were no more effective than the others. In cases caused by E. coli and Klebsiella, bacteriological cure was similar in treated and untreated cows.
• Rabiee and Lean (2013), meta-analysis of internal teat sealants containing bismuth subnitrate. Used alone or with antimicrobials at dry-off, they reduced new intramammary infections after calving by 25% (RR 0.75), and by 73% compared with untreated cows (RR 0.27), and reduced clinical mastitis by 29% to 48% depending on the comparison. Results for infections were highly heterogeneous.
• Winder et al. (2019), systematic review and meta-analysis of 9 trials comparing selective dry cow therapy with treatment of all cows. With selective therapy the risk of intramammary infection at calving was higher (RR 1.34), with substantial heterogeneity, but in the trials that used internal teat sealants there was no difference. The trials were few and did not allow clinical mastitis to be analysed.