-The objective of this study was to review the possible relationships between hyperketonemia and the function of phagocytes with respect to the bovine udder defense mechanism. We hypothesize that an increased incidence of clinical mastitis in high-producing cows is caused by the impairment of the udder defense mechanism during hyperketonemia. First, we review the acute phase of udder defense mechanisms after intramammary infection. The physiological changes of cows in negative energy balance are subsequently discussed. Finally, possible relationships between udder defense and physiological changes during negative energy balance, especially hyperketonemia, are reviewed. The three stages of an acute phase of udder defense are: (1) immediately eliminating invading pathogens by phagocytes, (2) releasing inflammatory substances, especially chemoattractants, and (3) migration of polymorphonuclear leukocytes into the infected udder. Leukocytes from hyperketonemia subjects show a lower capacity of the phagocytic defense mechanism. In addition, the phagocytic and bactericidal capacities of neutrophils are reduced when these cells are acting in the presence of high concentrations of ketone bodies. Lower amounts of cytokine production after bacterial infection are observed in ketotic subjects. The chemotactic capacity of blood leukocytes is impaired in leukocytes obtained from ketotic cows. Lower numbers of blood leukocytes are observed in ketotic cows. In conclusion, the impairment of the udder defense mechanism in negative energy balance cows seems related to hyperketonemia. ketosis / negative energy balance / mastitis / udder defense mechanism / cow Résumé -Hypercétonémie et diminution des défenses mammaires : une synthèse. L'objectif de cette étude est de présenter des relations possibles entre l'hypercétonémie et la fonction des phagocytes pour ce qui est des mécanismes de défense de la mamelle. Notre hypothèse est qu'une Vet. Res. 31 (2000) 397-412 397

A case-control study was conducted to evaluate factors measured at the udder inflammation-free state as risk factors for subsequent clinical mastitis. The factors including somatic cell count (SCC), body condition score, milk yield, percentages of milk fat and milk protein, and diseases were evaluated for their association with the results of udder inflammatory response. The results of the response were specified as presence (case) and absence (control) of clinical signs of mastitis. Data on Holstein Friesian cows calving from January 1984 to November 1996 from a commercial farm with low bulk milk SCC were used. Univariable and multivariable random-effect logistic models were used to evaluate the effect of those factors on the risk of clinical mastitis. The following variables were associated with increased odds of case versus control events in the univariable analysis: early lactation period, low SCC, high milk yield, high percentage of milk protein, high percentage of milk fat, low body condition score, retained placenta, and milk fever. For the final multivariable model of all variables used for analysis, only low SCC remained significantly associated with increased risk of subsequent clinical mastitis. The authors concluded that very low SCC during the udder inflammation-free state are associated with increased risk of clinical mastitis.

No abstract

No abstract

No abstract

The abilities of isolates to survive and be active in anaerobic and aerobic conditions rendered them to be active in cattle's rumen. Their biomass could be produced in bulk and used as feed supplement for aflatoxin detoxification in dairy cattle.

A longitudinal observational study was carried out to explore transmission dynamics and duration of infection of Streptococcus uberis. Quarter milk samples were collected aseptically for bacterial culture from all lactating cows once a month over a 10-mo period. Molecular typing of S. uberis mastitis was performed using pulsed-field gel electrophoresis (PFGE). Molecular typing was used to determine episodes of S. uberis intramammary infection (IMI). Comparisons of spontaneous cure among PFGE types were performed using Fisher's exact chi-squared tests. Differences of duration among PFGE types and between periods of lactation were tested with Kaplan-Meier survival curves and Cox's proportional hazard model. Among a total of 851 quarter samples, 145 milk samples were detected with S. uberis presence. Based on results of PFGE, 66 episodes of S. uberis IMI were determined. From the 8 main PFGE types (A-H), PFGE type D, E, F1, F2, G, and H had only one episode indicating no evidence for transmission, subsequently defined as environmental S. uberis strains. In contrast, PFGE types A1, A2, B, C1, and C2 had at least 2 infection episodes caused by the same strain in different quarters or cows, indicating that these strains would be able to transmit to other quarters or cows. These strains were defined as contagious strains. The majority of IMI were attributable to PFGE type A1 (55%), B (17%), and A2 (11%). Spontaneous cures were observed in 35 IMI episodes. Of these 35 IMI cures, 91.4% were in IMI with duration of infection of 1 mo, n = 25, and 2 mo, n = 6. The remaining 8.6% was in IMI with duration of infection >2 mo, n = 4. Based on results from Cox's proportional hazard model, environmental S. uberis episodes were likely to have spontaneous cure with shorter duration compared with contagious S. uberis with PFGE type B (hazard ratio = 8.4). Quarters infected with S. uberis strain PFGE type A in early lactation were more likely to persist compared with those infected in late lactation (hazard ratio = 7.57). In conclusion, the majority of S. uberis IMI in this herd were transient and showed spontaneous cure. In addition to environmental S. uberis IMI, at least 3 types of contagious IMI S. uberis can be defined as (1) short duration of IMI and likely to have spontaneous cure, (2) long duration and unlikely to have spontaneous cure, and (3) wide range of duration of IMI either transient or persistent where spontaneous cure may occur depending on host defense capacity.

A cross-sectional study was carried out from May to September 2011 on 35 smallholder dairy farms in Chiang Mai, Thailand, to identify the quarter, cow, and farm factors that relate to intramammary infections (IMI) from major specified pathogens, compared to infections from minor pathogens. Data on general farm management, milking management, and dry cow management were recorded for each herd. Quarter milk samples were collected from either clinical or subclinical mastitis quarters. Dependent variables were binary data defining the specified major pathogens, including Streptococcus agalactiae (7.1 %), Streptococcus uberis (9.4 %), Streptococcus dysgalactiae (4.0 %), and other streptococci (16.7 %), as a case, and all minor pathogens as a control, in each dependent variable. The occurrence of S. agalactiae IMI was lower in first-parity cows and cows with short milking time. Cows with body condition score (BCS) <2.5 had higher occurrence of S. agalactiae IMI. The occurrence of S. uberis IMI was higher in quarters with California mastitis test (CMT) score 2, score 3, and having clinical mastitis and in farms with increasing age of vacuum system. Quarters with CMT score 3, having clinical mastitis, cow with manual milking after detaching milking cluster, and farms with high bulk milk somatic cell counts (BMSCC >500,000 cells/ml) had higher occurrence of S. dysgalactiae IMI. For other streptococci, quarters having clinical mastitis, BCS <2.5, and pulling down of milking cluster while milking increased occurrence of other streptococci IMI relative to minor pathogen IMI. These results highlight the importance of individual cow factors, milking characteristics, and BMSCC in determining the risk of IMI from major pathogens.