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In this study, the contribution of management practices, herd characteristics, and seasonal variables to the herd somatic cell count (SCC) was quantified in herds with low (<150,000 cells/mL), medium (150,000- 200,000 cells/mL), and high (>200,000 cells/mL) herd SCC (HSCC). Selection of the variables was performed using a linear mixed effect model; HSCC was calculated as the arithmetic mean of the individual cow's SCC. The data concerning management practices were derived from 3 questionnaires on mastitis prevention and management practices on 246 Dutch dairy farms. The monthly Dairy Herd Improvement test data of these 246 farms were used to calculate the herd characteristics and seasonal effects. None of the management practices were associated with HSCC in all 3 HSCC categories. Some variables only had a significant association with HSCC in one HSCC category, such as dry premilking treatment (-9,100 cells/mL in the low HSCC category) or feeding calves with high SCC milk (11,100 cells/ mL in the medium HSCC category). Others had an opposite effect on HSCC in different HSCC categories, such as average parity ( 6,400 and 11,000 cells/mL in the low and medium HSCC category, respectively) and feeding calves with fresh milk (10,300 and -9,700 cells/ mL in the low and high HSCC category, respectively). We conclude that, given the individual Dairy Herd Improvement data and information on management practices of an individual farm, it is possible to provide quantitative insight into the contribution of these different variables to the HSCC of an individual farm. Being able to provide such insight is a prerequisite for interpretation, prediction, and control of HSCC on individual dairy farms. [ABSTRACT FROM AUTHOR]

The objective of this study was to assess growth of Escherichia coli in milk from endotoxin-induced mastitic quarters and to relate the in vitro findings to the course of experimental E. coli mastitis. Whole and skim milks from 24 rear quarters of 12 cows were inoculated with E. coli 0:157 and incubated at 38 degrees C. Growth of E. coli 0:157 was not inhibited in milk collected from rear quarters immediately prior to endotoxin infusion. However, growth inhibition occurred in all but one whole mastitic milk samples collected from mastitic quarters 18 h after infusion of .1 mg of endotoxin. Skim milk samples from mastitic quarters were bactericidal in four cows (7 quarters), whereas growth occurred in skim mastitic milk from 17 quarters of nine cows. Rear quarters of all cows were inoculated with 10(4) cfu of E. coli 0:157 19 h after the quarters had been infused with endotoxin. Clinical parameters and milk production were monitored during 36 h and 21 d, respectively. None of the inoculated quarters developed signs of inflammation, and secreta from inoculated quarters were bacteriologically negative after 48 h. Therefore, growth-inhibitory property of skim milk from endotoxin-induced quarters was apparently not a suitable parameter to monitor differences in susceptibility to E. coli mastitis.

The objectives were to describe the systemic signs during the acute phase of experimental Escherichia coli mastitis and to relate these with losses in milk production during the reconvalescent period. Eleven cows, 20 to 30 d postpartum, were inoculated with 10(4) cfu of E. coli O157 in rear quarters. Heart rate, rectal temperature, frequency and amplitude of rumen contractions, plasma Zn and Fe concentrations, and counts of E. coli were used to monitor severity of disease during the acute phase. Areas under curves of clinical parameters, plasma Zn and Fe concentrations, and counts of E. coli were calculated during 36, 120, and 125 h postinoculation, respectively. Areas under curves of milk production were calculated during 21 d postinoculation. Losses in total daily milk production were related positively with areas under curves of heart rate, rumen amplitude, counts of E. coli in secreta from inoculated quarters, and plasma Zn and Fe concentrations. These parameters may prove suitable to establish an accurate prognosis for returning to milk production cows suffering from acute or peracute E. coli mastitis and to evaluate efficacy of drugs in experimental mastitis.

The relationship between preinfection functions of blood neutrophils and outcome of experimental Escherichia coli mastitis was studied in 11 cows. Random migration, chemotaxis, phagocytosis, and chemiluminescence by neutrophils were determined in white blood cell suspensions, and in purified neutrophil suspensions. The course of E. coli mastitis (10(4) E. coli 0:157 in rear quarters) was monitored using clinical parameters, counts of E. coli in mastitic secretion, and milk production. Regressions were calculated for areas under curves of these parameters and preinfection activities of neutrophils. Chemiluminescence by nonstimulated neutrophils in white blood cell suspensions was negatively correlated with counts of E. coli in secretion and with losses in milk production. The chemotactic differential in white blood cell suspensions minus the chemotactic differential in purified suspensions of neutrophils referred to as delta varied from -.66 to +.50, indicating, respectively, inhibition and stimulation of chemotactic activity of neutrophils in white blood cell suspensions. Delta correlated negatively with counts of E. coli in mastitis secretion, inhibition of the amplitude of rumen contractions, and losses in milk production. We hypothesize that a factor in white blood cell suspensions may be involved in the down-regulation of the migratory response of neutrophils during E. coli mastitis.

Effects of intramammary infusion of prednisolone (40 mg) or intramuscular injection of dexamethasone (30 mg) or flumethasone (5 mg) on local and systemic signs in Escherichia coli endotoxin-induced mastitis were studied. The effect of varying intervals (0, 2, and 4 h) between intramammary infusion of endotoxin and prednisolone in the same quarter was determined. Intramammary infusion of endotoxin (.01 mg lipopolysaccharide of E. coli) produced inflammation of the infused quarter, fever, tachycardia, and leukopenia followed by a neutrophilic leukocytosis in the blood and a decrease in plasma zinc and iron concentrations. All corticosteroid treatments, except intramammary administration of prednisolone 4 h after endotoxin infusion, enhanced leukocytosis and diminished local signs of inflammation. Intramuscular injection of dexamethasone or flumethasone together with intramammary infusion of endotoxin and intramammary administration of prednisolone 2 h after lipopolysaccharide infusion completely abolished the febrile response. Abolishment of fever and attenuation of several hematologic and blood biochemical changes may be explained by diminished synthesis of endogenous mediators within the inflamed quarters due to glucocorticosteroid action.

A marked growth inhibition of Escherichia coli 0101 K99 F41 was observed in whole and skim milk collected from inflamed quarters 18 and 36 h after intramammary administration of .1 mg E. coli lipopolysaccharide. Individual cow variation in the ability of milk from endotoxin-infused quarters to inhibit growth of E. coli was found. Growth inhibition of E. coli was observed in milk from endotoxin-infused quarters and was most pronounced in skim milk sampled at postinfusion h 18, and incubated at 38 degrees C. The mechanism by which bacterial growth was depressed was probably of noncellular origin. Addition of Fe (45.5 micrograms/ml) and Zn (2.7 micrograms/ml) to whole and skim milk sampled from inflamed quarters at 18 h after endotoxin infusion resulted in a growth-promoting effect. Addition of deferoxamine (6 mg/ml) depressed bacterial growth. Effects of Fe, Zn, and deferoxamine on bacterial growth did not differ in whole and skim milk. No clear relationship was observed between reduction in Zn concentrations in skim milk from inflamed quarters at 18 h after endotoxin infusion and growth inhibition of E. coli in the same samples.

The effect of intramuscular administration of dexamethasone on milk production and on several clinical and hematologic indicators in cows with experimental Escherichia coli mastitis was studied. Two groups of three cows each were intramammarily inoculated with 20 x 10(5) cfu E. coli 0101 K99 F41 in rear quarters. Immediately after inoculation one groups received 30 mg dexamethasone intramuscularly, whereas the other group was injected similarly with pyrogen-free saline. Fourteen days later milk production losses were markedly less in the dexamethasone-treated group. Dexamethasone treatment reduced local clinical signs of inflammation, significantly increased rectal temperatures, and diminished inhibition of rumen amplitude during the acute phase of infection. Moreover, cows treated with dexamethasone showed diminished neutropenia, more pronounced hypozincemia, and delayed onset in the decrease in plasma iron concentrations. Possible mechanisms by which these changes are accomplished are discussed.