Results suggest that bacteremia develops in a substantial proportion of cows with ACM. Classification of severity of disease is important for establishment of effective treatment protocols; parenteral antimicrobial treatment may be indicated in cows with ACM.

Dairy cattle with clinical mastitis caused by Escherichia coli exhibit a wide range of disease severity, from mild, with only local inflammatory changes of the mammary gland, to severe, with significant systemic derangement. The present study was designed to examine the relationship between serotype and virulence genes of E. coli mastitis isolates, different levels of systemic disease severity, and farm from which the E. coli strain was obtained. One hundred twenty-three E. coli milk isolates were obtained from cows with clinical mastitis of varying systemic disease severity from 6 different farms. No predominant serotype was identified by farm or by systemic disease severity; however, the most frequent serotype, O158:NM (n = 3), was isolated from cows in the moderate severity group. Virulence genes evaluated were identified infrequently and were not associated with systemic disease severity. Evaluation of genetic similarity showed no clustering assigned by farm or mastitis severity based on systemic disease signs. We concluded that a high degree of genotypic variability is characteristic of E. coli strains causing clinical mastitis within and between different farms and systemic severity groups, and that specific cow factors probably play a more important role in determining systemic disease severity.

Results suggest that a classification scheme based on readily observable systemic disease signs can be used to classify disease severity in cows with acute coliform mastitis.

Daily evaluation of rectal temperature (RT) during the first 10 d in milk (DIM) is used to facilitate the early identification of postpartum complications, particularly metritis in dairy cows. The factors associated with RT of postpartum dairy cows have not been clearly established and the RT threshold used to define fever has been variable. The objectives were to identify factors associated with the RT of postpartum dairy cows and provide descriptive statistics of the RT during the first 10 DIM to clarify the normal range of RT for cows. Daily RT was evaluated from 1 to 10 DIM for all cows calving during 2 consecutive summers on a single 1,500-cow Holstein dairy. Cows were placed into metabolic/digestive (METB), infectious (INF), and no recorded disease (NONE) groups based on disease diagnoses during the first 10 DIM. Cows were grouped based on calving difficulty and parity. Multiple linear regression models with repeated measures were used to evaluate the factors associated with RT. Three hundred and ninety-two cows were evaluated, of which 45% were primiparous and 32% required assistance at calving. No difference was observed in calving assistance by parity. First disease diagnoses peaked in the INF and METB groups at 3 and 1 DIM, respectively. The RT of primiparous cows was 0.1 to 0.2°C higher than that of multiparous cows from 1 to 8 DIM, accounting for calving difficulty, twin births, month of calving, and disease group in the model. The INF group cows had a higher RT than did NONE group cows (38.9±0.04 to 39.2±0.73 vs. 38.7±0.03°C, respectively) on each of the first 10 DIM, which was approximately 0.6°C higher from 3 to 5 DIM. The RT of cows with metritis was at least 0.1°C higher (38.8±0.05°C) than that of NONE group cows beginning 4 d before diagnosis. The mean RT of primiparous, defined healthy (NONE group) cows was 38.8±0.02°C, with an upper normal limit (mean+2 SD) of 39.6°C. The mean RT of multiparous cows in the NONE group during the first 10 DIM was 38.7±0.01°C, with an upper normal limit of 39.5°C. The RT of dairy cattle during the first 10 DIM was associated with parity, month of calving, and an infectious disease diagnosis, particularly the diagnosis of metritis. The normal RT of dairy cattle in the immediate postpartum period, during the warm summer months, is potentially higher than that generally reported.

The objective of the current observational study was to determine the potential associations between cow factors, clinical mastitis (CM) etiology, and concentrations of select acute phase proteins and cytokines in milk from affected quarters of cows with CM. Cows with CM (n=197) were grouped based on systemic disease severity, milk culture result, parity, days in milk (DIM), previous CM occurrence, and season of the year when CM occurred. Concentrations of lipopolysaccharide-binding protein (LBP), haptoglobin (Hp), BSA, IFN-gamma, tumor necrosis factor-alpha (TNF-alpha), IL-1beta, IL-8, IL-10, IL-12, transforming growth factor (TGF)-alpha, and TGF-beta and activity of lactate dehydrogenase (LDH) were evaluated. Differences in the least squares means log(10) transformed concentrations of these proteins were compared using multiple linear regression mixed models. The milk concentrations of LBP, Hp, IL-1beta, IL-10, and IL-12, and activity of LDH in milk were higher in cows with moderate to severe versus mild systemic disease. The concentrations of Hp, BSA, IL-1beta, and IL-10 in milk were higher in cows with a gram-negative versus gram-positive milk culture result. Season of the year when CM occurred was associated with the concentration of all proteins evaluated except for IL-1beta and IL-12. Concentrations were higher in the winter versus summer except for Hp and TGF-beta, for which the opposite was true. Concentrations of LBP, IL-10, and IL-12, and LDH activity in milk were associated with DIM group. Except for LBP, these proteins were lower in cows with CM during the first 60 DIM versus those in mid or later lactation. Interferon-gamma, TNF-alpha, and IL-8 were undetectable in 67, 31, and 20% of samples, respectively. Detection of IFN-gamma and IL-8 was associated with season, and detection of TNF-alpha and IL-8 was associated with systemic disease severity. The current study provides the most comprehensive report of milk concentrations of innate immune response proteins in cows with naturally occurring CM and identifies factors that potentially influence those concentrations. Further investigation into the seasonal variation of cytokine production and its potential effect on the outcome of CM is warranted. Furthermore, the results of this study provide useful data for planning future studies examining the role of the innate immune response in CM.