Mastitis, inflammation of the bovine mammary gland, is generally caused by intramammary infection with bacteria, and antimicrobials have long been a corner stone of mastitis control. As societal concern about antimicrobial use in animal agriculture grows, there is pressure to reduce antimicrobial use in dairy farming. Point-of-care tests for on-farm use are increasingly available as tools to support this. In this Research Reflection, we consider available culture-dependent and culture-independent tests in the context of ASSURED criteria for low-resource settings, including convenience criteria, scientific criteria and societal criteria that can be used to evaluate test performance. As tests become more sophisticated and sensitive, we may be generating more data than we need. Special attention is given to the relationship between test outcomes and treatment decisions, including issues of diagnostic refinement, antimicrobial susceptibility testing, and detection of viable organisms. In addition, we explore the role of technology, big data and people in improved performance and uptake of point-of-care tests, recognising that societal barriers may limit uptake of available or future tests. Finally, we propose that the 3Rs of reduction, refinement and replacement, which have been used in an animal welfare context for many years, could be applied to antimicrobial use for mastitis control on dairy farms.

Mastitis is a costly disease and in many areas of the world, these costs have been quantified to support farmers in their decision making with regard to prevention of mastitis. Although for subsaharan circumstances estimates have been made for the costs of subclinical mastitis (SCM), farm-specific cost estimations comprising both clinical mastitis (CM) and SCM are lacking. In this paper, we quantified failure costs of both CM and SCM on 150 Ethiopian market-oriented dairy farms keeping Holstein Friesian × Zebu breed cows. Data about CM were collected by face-to-face interviews and the prevalence of SCM was estimated for each farm using the California mastitis test. All other relevant information needed to calculate the failure costs, such as the consequences of mastitis and price levels, was collected during the farm visits, except for the parameter for milk production losses due to SCM, which was based on literature estimates and subjected to sensitivity analyses. The average total failure costs of mastitis was estimated to be 4 765 Ethiopian Birr (ETB) (1 ETB = 0.0449 USD) per farm per year of which SCM contributed 54% of the costs. The average total failure costs per lactating cow per farm per year were 1 961 ETB, with a large variation between farms (range 0 to 35 084 ETB). This large variation in failure costs between farms was mainly driven by variation in incidence of CM and prevalence of SCM. Milk production losses made the largest contribution (80%), whereas culling contributed 13% to 17% to the total failure costs. In our estimates, costs of veterinary services, drugs, discarded milk and labour made a minor contribution to the total failure costs of mastitis. Relative to the income of dairy farmers in North Western Ethiopia; the total failure costs of mastitis are high. In general, Ethiopian farmers are aware of the negative consequences of CM, but creating awareness of the high costs of SCM and showing large variation between farmers may be instrumental in motivating farmers to also take preventive measures for SCM.

In 2010, a routine genetic evaluation on occurrence of clinical mastitis in three main dairy cattle breeds – Montbéliarde (MO), Normande (NO) and Holstein (HO) – was implemented in France. Records were clinical mastitis events reported by farmers to milk recording technicians and the analyzed trait was the binary variable describing the occurrence of a mastitis case within the first 150 days of the first three lactations. Genetic parameters of clinical mastitis were estimated for the three breeds. Low heritability estimates were found: between 2% and 4% depending on the breed. Despite its low heritability, the trait exhibits genetic variation so efficient genetic improvement is possible. Genetic correlations with other traits were estimated, showing large correlations (often>0.50, in absolute value) between clinical mastitis and somatic cell score (SCS), longevity and some udder traits. Correlation with milk yield was moderate and unfavorable (ρ=0.26 to 0.30). High milking speed was genetically associated with less mastitis in MO (ρ=−0.14) but with more mastitis in HO (ρ=0.18). A two-step approach was implemented for routine evaluation: first, a univariate evaluation based on a linear animal model with permanent environment effect led to pre-adjusted records (defined as records corrected for all non-genetic effects) and associated weights. These data were then combined with similar pre-adjusted records for others traits in a multiple trait BLUP animal model. The combined breeding values for clinical mastitis obtained are the official (published) ones. Mastitis estimated breeding values (EBV) were then combined with SCSs EBV into an udder health index, which receives a weight of 14.5% to 18.5% in the French total merit index (ISU) of the three breeds. Interbull genetic correlations for mastitis occurrence were very high (ρ=0.94) with Nordic countries, where much stricter recording systems exist reflecting a satisfactory quality of phenotypes as reported by the farmers. They were lower (around 0.80) with countries supplying SCS as a proxy for the international evaluation on clinical mastitis.

A total of 90 cows from three commercial farms were used to evaluate the relationship between subclinical mastitis and clinical mastitis and thermal nociceptive threshold. Milk strips from all udder quarters were tested for clinical mastitis with visual inspection of milk and udder alterations and for subclinical mastitis using California Mastitis Test. Milk yield was recorded, milk was sampled and further analyzed for somatic cells count (SCC). Cows were considered healthy when SCC<200 000 cells/ml and no visual alterations in milk and/or udder, with mild subclinical mastitis when SCC>200 000 cells/ml and no visual alterations in milk and/or udder, with moderate subclinical mastitis when SCC>500 000 cells/ml and no visual alterations in milk and/or udder and with clinical mastitis when visual alterations in milk and/or udder were detected. Nociceptive threshold was evaluated with the thermal threshold meter apparatus applied to the rear legs. Thermal threshold (TT) decreased when we compared healthy cows with cows presenting clinical mastitis and tended to decrease when we compare healthy cows with those with moderate subclinical mastitis. TT was lower at the ipsilateral rear leg compared with the contralateral leg to the infected mammary gland. TT linearly decreases as log10SCC increased and it showed sharp decrease as log10SCC exceed the value of 6.4. Increase in one unit of log10SCC increased the odds of low thermal threshold (lower than 55.8°C). Subclinical mastitis might be a welfare issue as it tended to decrease nociceptive thermal threshold.

Extended duration of clinical mastitis (CM) treatment has been advocated, although results showing its higher efficacy compared with standard treatment are difficult to compare and seem conflicting. In a non-blinded, positively controlled clinical trial with systematic allocation, the efficacy of a standard, 1·5-d cefquinome treatment (ST), and an extended, 5-d intramammary cefquinome treatment (ET) were evaluated. The latter is frequently performed in cows with persistent high somatic cell count (SCC), expecting a better cure. Therefore, cows with CM immediately preceded by at least two consecutive monthly elevated SCC >200 000 cells/ml, were studied. The primary efficacy criteria were bacteriological cure (BC) and clinical cure (CC), while SCC cure was considered a secondary criterion of cure. Least square means of overall BC were not different after ET (79%, n=206) compared with ST (72%, n=203). ET, as compared with ST, improved BC of CM when caused by streptococci, specifically Streptococcus uberis. At day 1·5, only 13% of quarters showed CC, increasing significantly towards 60% at day 5, and 99% at day 14 and at day 21. No significant difference in CC was present between treatment groups. Overall SCC cure was low (22%) and not significantly different between treatment groups, but significantly higher for cases due to enterobacteriacae compared with staphylococci. In conclusion, ET with cefquinome of CM in cows with a persistent high SCC seems to be only indicated when caused by streptococci, mainly Str. uberis but shows no advantage when no information on bacteriological causes of mastitis is available. In our data, absence of CC directly after ST was not related to eventual BC.

The objective of this clinical control trial was to examine the effectiveness of the classical homeopathic treatment strategy in cases of mild and moderate bovine clinical mastitis in comparison with antibiotic and placebo treatments. Owing to characteristics of the selected herds, only cases of clinical mastitis caused by environmental pathogens and clinical cases with negative bacteriological result in the pre-treatment milk sample were included in the trial. A total of 136 lactating dairy cows with 147 affected quarters from four herds in Germany were randomly allocated to three treatment groups. The cows were examined on days 0, 1, 2 and on days 7, 14, 28 and 56 post initial infection to assess clinical signs. Simultaneously, with the exception of days 1 and 2, quarter milk samples for laboratory examinations (bacteriology, somatic cell count) were collected to assess bacteriological and cytological cure rates. On days 28 and 56, treatment strategies did not differ significantly with respect to the clinical outcomes and the total cure rate in cases of bacteriological negative mastitis (n=56). In cases of pathogen-positive mastitis (n=91), the cure rate after 4 and 8 weeks was similar between the two treatment strategies, homeopathy and antibiotic treatment, but the difference between the homeopathic and the placebo treatment at day 56 was significant (P<0·05). The results indicate a therapeutic effect of homeopathic treatment in cases of mild and moderate clinical mastitis. However, independent of treatment strategy and bacteriological status, the total cure rate was on a low level, revealing limitations in the effectiveness of both antibiotic and homeopathic treatment strategies.

A genetic analysis of longitudinal binary clinical mastitis (CM) data recorded on about 90 000 first-lactation Swedish Holstein cows was carried out using linear random regression models (RRM). This method for genetic evaluation of CM has theoretical advantages compared to the method of linear cross-sectional models (CSM), which is currently being used. The aim of this study was to investigate the feasibility and suitability of estimating genetic parameters and predicting breeding values for CM with a linear sire RRM. For validation purposes, the estimates and predictions from the RRM were compared to those from linear sire longitudinal multivariate models (LMVM) and CSM. For each cow, the period from 10 days before to 241 days after calving was divided into four 1-week intervals followed by eight 4-week intervals. Within each interval, presence or absence of CM was scored as ‘1’ or ‘0’. The linear RRM used to explain the trajectory of CM over time included a set of explanatory variables plus a third-order Legendre polynomial function of time for the sire effect. The time-dependent heritabilities and genetic correlations from the chosen RRM corresponded fairly well with estimates obtained from the linear LMVM for the separate intervals. Some discrepancy between the two methods was observed, with the more unstable results being obtained from the linear LMVM. Both methods indicated clearly that CM was not genetically the same trait throughout lactation. The correlations between predicted sire breeding values from the RRM, summarized over different time periods, and from linear CSM were rather high. They were, however, less than unity (0.74 to 0.96), which indicated some re-ranking of sires. Sire curves based on the time-specific breeding values from the RRM illustrated differences in intercept and slope among the best and the worst sires. To conclude, a linear sire RRM seemed to work well for genetic evaluation purposes, but was sensitive for estimation of genetic parameters.

The main aim of the present study was to examine the economic consequences of a reduction in the incidence of clinical mastitis (CM) at herd level under current Swedish farming conditions. A second objective was to ask whether the estimated cost of CM alters depending upon whether the model reflects the fact that in different stages of lactation, CM gives rise to different yield-loss patterns or postulates just one type of yield-loss pattern irrespective of when, during lactation, CM occurs. A dynamic and stochastic simulation model, SimHerd, was used to study the effects of CM in a herd with 150 cows (9000 kg of energy-corrected milk per cow-year). Four herd types, defined by production level and reproductive performance, were modelled to investigate possible interactions between herd type and response to a reduction in the risk of CM. Technical and economic results, given the initial incidence of CM (25.6 per 100 cow-years), were studied together with the consequences of reducing the initial risk of CM by 50% and 90% throughout lactation and the consequences of reducing the initial risk by 50% and 90% before peak yield. A conventional way of modelling yield losses – i.e. one employing a single yield-loss pattern irrespective of when, during the lactation period, the cow develops CM – was compared with a new modelling strategy in which CM was assumed to affect production differently depending on its lactational timing. The effect of the choice of reference level when estimating yield losses was investigated by comparing the results obtained using the potential yield of mastitic cows, had they not developed CM, with those obtained using the yield of non-mastitic cows. The yearly maximum avoidable cost of CM at herd level was estimated at €14 504, corresponding to 6.9% of the net return given the initial incidence of CM. Expressed per cow-year, the maximum avoidable cost was €97. The cost per case of CM was estimated at €428. Herd types all responded in a similar manner to the reduced relative risk of CM. There were no major differences in the results obtained using the new and the conventional modelling strategy, with the exception of the cost per case of CM. Similarities between the results obtained using the two methods were particularly evident when the mastitic cows’ own yield level, had they not developed CM, was used as the reference for production in healthy cows when yield losses were estimated. It was concluded that the conventional way of modelling yield losses is adequate and should, for the foreseeable future, be used in decision support systems.

Cows with isolation of Staphylococcus aureus approximately 1 week after calving and milk yield, somatic cell count (SCC), clinical mastitis (CM), and culling risk through the remaining lactation were assessed in 178 Norwegian dairy herds. Mixed models with repeated measures were used to compare milk yield and SCC, and survival analyses were used to estimate the hazard ratio for CM and culling. On average, cows with an isolate of Staph. aureus had a significantly higher SCC than culture-negative cows. If no post-milking teat disinfection (PMTD) was used, the mean values of SCC were 42 000, 61 000, 68 000 and 77 000 cells/ml for cows with no Staph. aureus isolate, with Staph. aureus isolated in 1 quarter, in 2 quarters and more than 2 quarters respectively. If iodine PMTD was used, SCC means were 36 000; 63 000; 70 000 and 122 000, respectively. Primiparous cows testing positive for Staph. aureus had the same milk yield curve as culture-negative cows, except for those with Staph. aureus isolated in more than 2 quarters. They produced 229 kg less during a 305-d lactation. Multiparous cows with isolation of Staph. aureus in at least 1 quarter produced 94–161 kg less milk in 2nd and >3rd parity, respectively, and those with isolation in more than 2 quarters produced 303–390 kg less than multiparous culture-negative animals during a 305-d lactation. Compared with culture-negative cows, the hazard ratio for CM and culling in cows with isolation of Staph. aureus in at least 1 quarter was 2·0 (1·6–2·4) and 1·7 (1·5–1·9), respectively. There was a decrease in the SCC and in the CM risk in culture-negative cows where iodine PMTD had been used, indicating that iodine PMTD has a preventive effect on already healthy cows. For cows testing positive for Staph. aureus in more than 2 quarters at calving, iodine PMTD had a negative effect on the CM risk and on the SCC through the remaining lactation.

Data from 350 herds enrolled in the Norwegian Dairy Herd Recording System (NDHRS) were used to investigate the associations between the first two cow-milk somatic cell counts (SCC) test-days’ results after calving or the three last SCC test-days prior to drying off in the first lactation and the hazard ratio (HR) of clinical mastitis (CM) during the remaining first or the subsequent second lactation respectively. Altogether, 9519 first lactations and 6046 second lactations were included. Cox regression analyses adjusted for herd frailty effect were used. In the first lactation, SCC>40000 cells/ml on the first or second test-day was significantly associated with an increased risk of a CM event in the remaining first lactation. HR, compared with 10000 cells/ml, increased from 1·6 (1·4) for SCC of 40000–60000 cells/ml to 6·9 (4·2) for SCC >800000 cells/ml, when using the first (second) SCC test-day in the first lactation. Cows with a geometric mean of the three last SCC test-days between 50000 and 100000 cells/ml and between 401000 and 800000 cells/ml in the first lactation had HR of CM during the second lactation of 1·3 and 2·8 respectively compared with a reference group of 10000–20000 cells/ml. If a CM episode in the first lactation occurred, the HR for having a CM event during the second lactation was 1·5. There was a significant frailty effect which disappeared if the incidence rate of CM at herd level was included in the model.

Clinical mastitis records on 36 178 first-lactation Norwegian dairy cattle (NRF) cows, daughters of 245 sires from 5286 herds, were analysed to study the impact of trait definition on estimates of genetic parameters and sire evaluations for clinical mastitis. The opportunity interval for infection, going from 30 days pre-calving to 300 days post partum, was divided into either 11 periods (each 30 days long); four periods ((-30, 0), (1, 30), (31, 120), (121, 300)); a single period (-30, 300) or defined as the interval currently used for sire evaluation in Norway (-15,120). Within each period, clinical mastitis was scored as 1 if it occurred at least once and 0 otherwise. Analysis was with Bayesian threshold models, assuming that mastitis (presence v. absence) was a different trait in each period. By use of multivariate or univariate normal link functions, unobserved liabilities to disease were modelled as a linear function of year of calving, age-season of calving, herd, sire of cow and residual effects. Estimates of heritability of liability to clinical mastitis ranged from 0-06 to 0-14, depending on the model and stage of lactation. In multi-period models, estimates of genetic correlations between periods were positive and ranged from 0-13 to 0-55. This suggests that clinical mastitis resistance is not the same trait in different periods of the first lactation, which is not captured by the single-interval models. The single-interval (-30, 300) model gave slightly smaller sire-specific posterior probabilities of clinical mastitis during the first lactation than the multi-period models. Furthermore, the interval used in current Norwegian sire evaluation understated the posterior probabilities of clinical mastitis, relative to the multi-period specifications. This led to some differences in sire rankings between the four models, although there was agreement between the four- and 11-period models. In conclusion, the multi-period models captured more genetic variation than the single-interval models, but the four-period model gave sire rankings that differed little from those obtained with an 11-period definition of clinical mastitis.