An ELISA has been developed for measurement of milk and serum IgG concentrations directed against Salmonella dublin. Four groups of cows were studied: group A-7 experimentally challenge-exposed cows (infected, recovered group); group B-6 normal uninfected randomly selected control cows; group C-7 naturally occurring S dublin carrier cows; and group D-6 normal uninfected S dublin negative cows from the same herd as group C. Group-A cows were inoculated orally, or inoculated orally and then IV, but none became a S dublin carrier. As expected, all 7 group-A cows responded with a marked increase in ELISA titer after oral exposure to virulent S dublin, starting with a mean serum titer of 17.7% and reaching a peak mean serum titer of 79.3% approximately 76 days after initial exposure. As determined by necropsy and organ culturing of the remaining cows, none of the group-A cows became carriers. The mean serum ELISA titer for group-B uninfected control cows was 14.1% (SD +/- 12.8%). The mean milk ELISA titer was -1.0% (SD +/- 5.5%). Colostrum and then milk gave false-positive results for up to 2 weeks after onset of lactation. Group-B cows were culture negative for S dublin in feces and milk during lactation, and when tissues were cultured after euthanasia. Milk and serum samples for ELISA, and milk and fecal samples for culturing were taken from all group-A and -B cows twice a week for 6 months. Statistical correlation (P less than 0.05) was found between serum and milk ELISA titers. A highly significant (P less than 0.001) difference in serum ELISA titers was demonstrated between control (group B) and infected cows (group A). Milk and feces from group-C carrier cows were cultured for S dublin 5 days a week for 11 to 13 months. Six of the 7 cows calved during this period. Fecal shedding was sporadic in 7 cows. Milk shedding was frequent in certain quarters of 4 of the cows and was sporadic or absent in other quarters of these cows and it was sporadic in 2 cows, and 1 cow had culture-positive milk only twice. The overall milk-shedding rate was 46% (792 positives/1,733 samples), whereas the overall fecal-shedding rate was 4% (65 positives/1,733 samples). Shedding in the 4 weeks after parturition was 28% in milk and 5% in feces. Six group-C cows had strongly positive ELISA titers in serum and milk, whereas 1 cow (the cow that had only 2 positive milk cultures) had relatively low ELISA titers. Group-C cows had a mean serum titer of 85.2% (SD +/- 19%) and mean milk titer of 70.6% (SD +/- 35.5%). These results indicate that IgG ELISA may be useful in detection of S dublin milk shedding (mammary gland infection) carrier cows. Milk shedding in the 4 persistent shedders ranged from 10(1) to 10(5) organisms/ml, and was associated with evidence of chronic active mastitis. Group-D cows, culture-negative herd mates of group-C carrier cows, were monitored in a manner identical to that used for group-C cows. All cows remained culture-negative for S dublin in feces and milk and results of organ culturing were negative for S dublin after euthanasia. The ELISA titers remained negative, with a mean group-D titer of 8 +/- 7.7% on serum, and 0.6 +/- 5.5% on milk. A highly significant difference in serum (P less than 0.0001) and milk (P less than 0.0001) ELISA titers was demonstrated between group-C carrier cows and group-D uninfected herd mates.

The effect of aspirin on bovine platelet function and thromboxane A2 (TXA2) production in stimulated platelets was evaluated. A single dose of aspirin (100 mg/kg of body weight) was administered orally to Holstein cows, and blood samples were obtained before and at regular intervals for 7 days after treatment. The production of TXA2 was assessed by measuring the stable metabolite thromboxane B2, using a specific radioimmunoassay. Within 4 hours of aspirin administration, the production of TXA2 was significantly (P less than 0.05) decreased, irrespective of whether collagen, adenosine diphosphate, or platelet activating factor was used to initiate platelet aggregation. Despite the inhibition of TXA2 release from the stimulated platelets, platelet function, assessed by initial rate of aggregate formation and extent of aggregation, was unaffected by aspirin administration. The extent of aggregate formation in response to collagen, adenosine diphosphate, or platelet activating factor was independent of the amount of TXA2 released from platelets before and after aspirin treatment. The results suggested that TXA2 formation is not the primary biochemical pathway involved in the aggregation of stimulated bovine platelets.

Functional capabilities of morphologically mature (segmented) and immature granulocytes (neutrophils and eosinophils) from bone marrow from cows were studied and compared with similar activities of segmented granulocytes from blood. Phagocytosis of Escherichia coli and postphagocytic oxidative metabolic stimulation, measured by nitroblue tetrazolium (NBT) reduction, were evaluated simultaneously. Phagocytosis was observed readily in segmented neutrophils, neutrophilic bands, and metamyelocytes and rarely in myelocytes. Phagocytosis was not seen in promyelocytes and myeloblasts. Neutrophilic bands and metamyelocytes were phagocytically less active than were segmented neutrophils. Washed segmented bone marrow neutrophils possessed phagocytic activity similar to that of blood neutrophils, whereas the activity of unwashed segmented bone marrow neutrophils was markedly less than that of blood neutrophils. Reduction of NBT was observed only in blood segmented neutrophils and bone marrow segmented neutrophils; the magnitude of NBT reduction was significantly (P = less than 0.005) less in bone marrow neutrophils than in blood neutrophils. Eosinophils were phagocytically less competent than were neutrophils. The NBT reduction was observed only in eosinophils from blood, but not in eosinophils from bone marrow.

Eight adult Holstein cows were used to compare the effects of lumbar segmental epidural analgesia (SEA) and lumbar segmental subarachnoid analgesia (SSA). A modified 17-gauge Huber point (Tuohy) needle was used to place a catheter with stylet into either the epidural space at the thoracolumbar (T13-L1) intervertebral space or the tubarachnoid space at the lumbosacral intervertebral junction. The catheters were advanced so that their tips lay at the anterior lumbar (L1-L2) epidural space or at the thoracolumbar (T-13-L1) subarachnoid space. The position of the catheter was confirmed radiographically. A 5% solution of procaine HCl was used at mean doses of 300 mg (6 ml) to induce SEA and 84.4 +/- 12.9 mg (1.7 +/-0.3 ml) to induce SSA. Onset of analgesia to superficial and deep muscular pinprick stimulation was significantly (P less than 0.05) faster in cows with SSA than in those with SEA (10.4 +/- 2.3 minutes vs 15.9 +/- 3.8 minutes). Maximal thoracolumbar analgesia extended from spinal cord segments T12 to L4 on one or both sides of the vertebral column during SEA and from T10 to L3 on one or both sides during SSA. Duration of analgesia lasted significantly (P less than 0.05) longer in cows with SEA than in those with SSA (76.2 +/- 16.2 minutes vs 53.7 +/- 14.3 minutes). The advantages and disadvantages of the SEA catheter technique are discussed.

Ovariectomized, nonlactating cows were treated with IM injections of either physiologic saline solution or prostaglandin F2 alpha. Plasma concentrations of cortisol increased significantly by 30 to 60 minutes after injection of prostaglandin F2 alpha, but there were no significant increases in plasma concentrations of estradiol, progesterone, or testosterone. After saline solution treatment, there were no increases in any of the hormones measured.

Mastitis was induced in 4 lactating cows by inoculation of Klebsiella pneumoniae (10(7) organisms/ml) via the teat canal. Sterile isotonic saline solution (1 ml) was instilled into designated control quarters via the teat canal. Changes in milk leukotriene B4 and C4 (LTB4, LTC4) concentrations, milk somatic cell counts, and milk bovine serum albumin concentration were monitored over a 24-hour postinoculation period. Milk LTB4 concentration before inoculation in control quarters and quarters later to be infected was 376 +/- 45 and 326 +/- 56 pg/ml of milk, respectively. A significant (P less than 0.05) increase in milk LTB4 concentration in the infected quarters was first observed at postinoculation hour 6, and milk LTB4 concentration in infected quarters generally remained significantly high through postinoculation hour 14. Thereafter, milk LTB4 concentration in infected quarters was not significantly different from the concentration in control quarters. Measurable amounts of LTC4 were not detected in the milk of either control or infected quarters. Milk bovine serum albumin concentration in the infected quarters generally was high throughout the study, as were milk somatic cell counts. The results of this study suggested that LTB4 contributes to the pathogenesis of bovine mastitis.

Blood and urine chemical values at parturition in clinically normal Holstein cows (n = 12) were compared with the same values in Holstein cows developing udder edema (n = 12). There was no statistically significant mean difference between the 2 groups for the serum and urine chemical data. Furosemide (500 mg) given IV caused a significant increase in serum calcium and sodium, urine chloride, potassium, and sodium, and fractional excretional ratio of chloride, potassium, and sodium. There was a significant mean decrease in the serum potassium, urine creatinine, osmolality, pH, and specific gravity. Hydrochlorothiazide (250 mg) given IV caused a significant mean increase in serum chloride, urine chloride, potassium, and sodium, and fractional excretion ratio of chloride, potassium, and sodium. There was a significant mean decrease in serum potassium and sodium, urine osmolality, pH, and specific gravity. Acetazolamide (500 mg) given IV caused a significant mean increase in blood urea nitrogen, serum chloride and glucose, urine sodium, and fractional excretion ratio of sodium, while causing a significant mean decrease in serum potassium, sodium, and phosphorus, and urine creatinine. Dextrose (500 g) given IV as a 50% solution caused a statistical mean increase in serum glucose, urine chloride, potassium, and sodium, and fractional excretion ratio of chloride and potassium. A statistical mean decrease occurred in the packed cell volume, blood urea nitrogen, serum calcium, potassium, sodium, and phosphorus, urine creatinine, osmolality, and pH.

Ten Holstein heifers were fed a selenium-deficient (SeD) diet (0.04 mg of Se/kg on a total ration dry-matter basis) 3 months before calving and throughout their first lactation. A selenium-supplemented (SeS) diet (2 mg of Se/head/d) was fed to a group of 10 heifers. In about the 14th week of lactation, the cows were challenge-exposed to Escherichia coli by administering 15 to 40 colony-forming units (CFU) into 1 mammary gland. Selenium concentration microgram/ml) in blood around the time of challenge exposure was 0.033 +/-0.002 (mean +/- SEM) in SeD and 0.132 /-0.006 in SeS cows. Infections were established in all challenge-exposed quarters. The frequency of quarter atrophy and agalactia, and reduction in whole-udder milk yield in the first 4 days after challenge exposure, were greater (P < 0.05) in the SeD cows. Log10 peak bacterial concentrations in milk were higher (P < 0.05) in SeD (7.63 +/- 0.34 CFU/ml) than in SeS cows (5.57 0.66 CFU/ml). Mean log bacterial concentration was significantly higher (P < 0.05) from 12 to 20 hours after challenge exposure in SeD than in SeS cows. Duration of infection was significantly greater (P < 0.05) in SeD (162.0 +/- 12.0) than in SeS cows (114.4 +/- 18.0 hours). Milk somatic cell counts increased significantly more slowly (P < 0.05) in SeD than in SeS cows from 8 to 16 hours after challenge exposure. Ratios of milk somatic cells to bacteria in milk were significantly lower (P < 0.05) in SeD than in SeS cows at l2 and 16 hours after challenge exposure.