Foremilk, residual milk, and blood samples were studied for 10 days during acute mastitis episodes induced by endotoxin infused via the teat canal. Quarter milk and blood samples were collected frequently for 3 days after the infusion and thereafter once or twice daily. Leukocyte concentration in milk and blood was determined by flow cytometry. Within 2 hours after infusion of the endotoxin, clinical mastitis was observed. Total leukocyte concentration and proportion of neutrophils increased significantly (P < 0.05) by postinfusion hour (PIH) 2 in foremilk and by PIH 4 in residual milk. From PIH 2, serum albumin content and N-acetyl-beta-D-glucosaminidase activity were significantly increased in both fractions. Neutrophils were the predominant leukocyte population in both fractions until PIH 59. From PIH 72, lymphocytes were the predominant cell population until PIH 175 in foremilk and until PIH 223 in residual milk. Serum albumin content and N-acetyl-beta-D-glucosaminidase activity in residual milk was significantly lower than in foremilk from PIH 4 to 24 and from PIH 24 to 59, respectively. Regarding total and differential leukocyte counts, values for the 2 fractions followed the same pattern throughout the course of inflammation, probably owing to frequent sample collection. Total and differential cell counts tended to differ between the fractions during some periods, although differences were not statistically significant. When samples were taken less frequently, the total leukocyte concentration in residual milk was higher than that in foremilk. Although sample collections were frequent, clustering of immature neutrophils was not observed in the cytofluorogram of blood leukocytes in this study. Residual milk seems to be the fraction that best reflects the condition in the quarter at the particular time when the milk sample is taken. Results also indicate that residual milk reflects the condition of the secretory tissue, as well as the lower regions of the gland.

The role of interleukin-1 (IL-1), interleukin-6 (IL-6), and tumor necrosis factor a during endotoxin-induced mastitis in cows was characterized. Six cows had 10 microgram of Escherichia coli lipopolysaccharide infused into 1 mammary gland. Three other cows served as nontreated controls. Within 1.5 to 2.5 hours after infusion, endotoxin caused obvious edema of the mammary gland and increased serum albumin concentration in milk of infused glands 6 times. Milk somatic cell count began to increase 3 to 5 hours after infusion in all treated glands. At 7 hours after infusion, somatic cell counts were increased > 10 times, compared with counts in milk from control cows. Pyrexia of > 1 C developed in only 1 cow, but all treated cows had serum cortisol concentrations > 50 ng/ml in response to endotoxin treatment. High concentrations of IL-1 (10 to 600 U/ml) and IL-6 (2 to 22 U/ml) were detected in milk of infused glands beginning 2.5 to 4 hours after infusion. Endotoxin did not induce detectable amounts of tumor necrosis factor activity in milk or serum. Swelling and mammary gland permeability changes preceded any detectable increase in IL-1 and IL-6 activity, indicating that these clinical signs of inflammation were not mediated by these cytokines. Systemic responses and the leukocytic influx into endotoxin-infused glands developed after or concurrently with initial increases in IL-1 and IL-6 activities in milk. These results suggested that IL-1 and IL-6 may have a role in mammary gland defenses and in the pathophysiologic changes during endotoxin-induced mastitis.

Estradiol was administered to 3 steers (0.12 mg/kg of body weight/d for 14 consecutive days), followed by 2 days of nonfeeding (starvation). During estradiol administration, liver nuclear estrogen receptor and serum apolipoprotein B-100 (apoB-100), as well as serum triglycerides concentrations were increased, compared with values before administration. Starvation, together with interruption of estradiol administration, resulted in rapid decreases of the receptor, serum apoB-100, and serum triglycerides concentrations, and increase of nonesterified fatty acids concentration. Of the 3 steers, 2 had higher liver triglyceride content, compared with values before treatment. In the control group (3 steers that received vehicle alone, then starved similarly), these concentrations, except for serum nonesterified fatty acids and triglycerides concentrations after starvation, were not changed. In another experiment, serum apoB-100 concentration in dairy cows was significantly (P < 0.05) lower at parturition than values before and after parturition. These results indicate that estradiol may be involved in development of fatty liver in cattle.

Cows and calves from a 1,600-cow drylot dairy were screened for IgG antibodies to Salmonella dublin lipopolysaccharide (LPS), using an indirect ELISA. The ELISA was performed on milk samples from lactating cows and on sera from nonlactating cows and calves. Fecal samples were collected from calves and nonlactating cows for culture of Salmonella spp. All seropositive cattle were retested by culture and ELISA 5 times at monthly intervals or until antibody concentration decreased. None of the cattle remained culture-positive and seronegative. Prior to and during the sample collection period, approximately 30% of calves < 8 weeks old died of S dublin infection. Vaccination of cows with a killed S dublin/S typhimurium vaccine at cessation of lactation was a routine management practice. The ELISA-determined Igg response to vaccination had decreased by 50 days after vaccination. Eight cows and 5 calves that maintained a high serologic response to S dublin were purchased and moved to a research facility for 6 months of intensive monitoring. Lactating cows were milked twice daily, and culture of milk and feces for Salmonella spp was performed 5 times/wk. Serum IgG antibodies to S dublin LPS were measured weekly, using ELISA. At the end of 6 months, all 13 cattle were necropsied and tissues were obtained for culture of Salmonella spp. All 8 cows and 5 calves maintained persistently high ELISA titer for the 6 months of testing, and shed S dublin in the milk and/or feces during the same period. On this basis, they were termed S dublin carriers. Salmonella dublin was isolated from mammary tissue of 2 calves at necropsy, indicating that bacteremia may be a mode of mammary infection by S dublin. Results of the study indicated serologic testing can be used successfully on a large dairy to identify S dublin carrier cattle. Using initial milk screening, 42 of 1,268 lactating cows were identified as suspect, requiring repeated serologic testing. One nonlactating cow, 7 of the 42 suspect lactating cows, and 5 of the 222 calves maintained an Igg response, and were found to be S dublin carriers. Carrier cows shed S dublin in 3.35% of fecal samples and 2.51% of milk samples, and carrier calves shed S dublin in 17.26% of fecal samples.

The role of interleukin-1 (IL-1), interleukin-6 (IL-6), and tumor necrosis factor a during endotoxin-induced mastitis in cows was characterized. Six cows had 10 microgram of Escherichia coli lipopolysaccharide infused into 1 mammary gland. Three other cows served as nontreated controls. Within 1.5 to 2.5 hours after infusion, endotoxin caused obvious edema of the mammary gland and increased serum albumin concentration in milk of infused glands 6 times. Milk somatic cell count began to increase 3 to 5 hours after infusion in all treated glands. At 7 hours after infusion, somatic cell counts were increased > 10 times, compared with counts in milk from control cows. Pyrexia of > 1 C developed in only 1 cow, but all treated cows had serum cortisol concentrations > 50 ng/ml in response to endotoxin treatment. High concentrations of IL-1 (10 to 600 U/ml) and IL-6 (2 to 22 U/ml) were detected in milk of infused glands beginning 2.5 to 4 hours after infusion. Endotoxin did not induce detectable amounts of tumor necrosis factor activity in milk or serum. Swelling and mammary gland permeability changes preceded any detectable increase in IL-1 and IL-6 activity, indicating that these clinical signs of inflammation were not mediated by these cytokines. Systemic responses and the leukocytic influx into endotoxin-infused glands developed after or concurrently with initial increases in IL-1 and IL-6 activities in milk. These results suggested that IL-1 and IL-6 may have a role in mammary gland defenses and in the pathophysiologic changes during endotoxin-induced mastitis.

In vitro transferability of penicillin, streptomycin, tetracycline, and erythromycin resistance from coagulase-negative staphylococci to Staphylococcus aureus and among the former species of bovine mammary gland origin was examined by bacterial mating on filters and by mixed-culture matings in broth and in skim milk. One hundred twenty-six (42 each on filter, in broth, and in skim milk) matings were performed among 37 isolates of different Staphylococcus species. Transfer of resistance to penicillin, tetracycline, or erythromycin was not detected. Of 51 matings performed to determine streptomycin-resistance transfer, 9 (3 each on filters, in broth, and skim milk) were successful. Nine strains representing 3 species of coagulase-negative staphylococci were tested as prospective donors of streptomycin resistance. Of these, 2 strains could transfer streptomycin resistance. A double-resistant donor, S hominis, not only transferred its streptomycin resistance to an S chromogenes strain lacking resistance, but also to an S aureus strain already carrying penicillin and tetracycline resistance. The transfer of streptomycin resistance from the donor S hominis, harboring 2 plasmids, to a plasmidless S chromogenes recipient strain was associated with apparent acquisition of the smaller plasmid of the donor by the recipient. The single-resistant donor, S epidermidis 681A, transferred streptomycin resistance to a tetracycline-resistant S aureus recipient. This strain however, failed to transfer its streptomycin resistance to another S aureus, 2 S hyicus, and 1 S xylosus recipient. Frequency of transfer of streptomycin resistance ranged from 1.1 X 10(-5) to 1 X 10(-4). When transfer of resistance was successful, attempts were made to characterize the transfer process. Conjugation appeared to be the mode of streptomycin-resistance transfer. Transfer of resistance between staphylococci of bovine mammary gland origin appears to be fairly uncommon. However, in view of the limitations of the procedures used, additional in vitro and in vivo work is needed to further assess the role of coagulase-negative staphylococci in dissemination of antibiotic resistance.

Approximately 45 Holstein cows that were Mycobacterium paratuberculosis-positive on the basis of fecal culture results were maintained at any one time in a 210-cow dairy herd. Farm management participated in the New York State Paratuberculosis Eradication Program. Paratuberculosis-positive cows were grouped separately from paratuberculosis-negative cows, but they were otherwise managed identically. During a 1-year study, 180 paratuberculosis-negative cows and 113 clinically normal paratuberculosis-positive cows were identified. Quarter milk samples (n = 6,100) were aseptically collected for microbiologic culture of mastitis pathogens from paratuberculosis-negative cows, and 3,129 quarter samples were obtained from paratuberculosis-positive cows. Dairy Herd Improvement Association (DHIA) records were used to monitor milk somatic cell count linear scores, mature equivalent milk production, new mastitis infections, and chronic mastitis infections. For second-lactation cows greater than 100 days in milk production, and increasing with age beyond that point, paratuberculosis-positive cows had lower mature equivalent milk production than did negative herdmates. Rates of new and chronic mastitis infections, as measured by DHIA linear scores were significantly (P less than 0.05, P = 0.05, respectively) lower in cows with nonclinical paratuberculosis. Infected cows were cuffed from the herd at a faster rate than were paratuberculosis-negative herdmates. Therefore, paratuberculosis was associated with financial loss attributable to reduced milk production and increased culling of infected cows.

Effects of a change from a diet composed primarily of forage to a diet composed primarily of concentrate on abomasal antral and duodenal motility were assessed in 5 lactating Holstein cows. Antroduodenal motility was measured by use of 8 silver electrodes sutured to ther abomasum and duodenum, and abomasal emptying was assesssed by continuous measurement of intraduodenal pH. Both diets were fed to achieve a daily dry matter intake of 2.7 kg/100 kg of body weight. The abrupt change in diet did not alter antoduodenal myoelectric activity or abomasal emptying. Initiation of phase III of the migrating myoelectric complex in the proximal portion of the duodenum corresponded with a decrease in abomasal antral spiking activity and an increase in intraduodenal pH. Results suggest that a high concentrate diet alone does not adversely affect antroduodenal motility in adult dairy cattle.

Foremilk, residual milk, and blood samples were studied for 10 days during acute mastitis episodes induced by endotoxin infused via the teat canal. Quarter milk and blood samples were collected frequently for 3 days after the infusion and thereafter once or twice daily. Leukocyte concentration in milk and blood was determined by flow cytometry. Within 2 hours after infusion of the endotoxin, clinical mastitis was observed. Total leukocyte concentration and proportion of neutrophils increased significantly (P < 0.05) by postinfusion hour (PIH) 2 in foremilk and by PIH 4 in residual milk. From PIH 2, serum albumin content and N-acetyl-beta-D-glucosaminidase activity were significantly increased in both fractions. Neutrophils were the predominant leukocyte population in both fractions until PIH 59. From PIH 72, lymphocytes were the predominant cell population until PIH 175 in foremilk and until PIH 223 in residual milk. Serum albumin content and N-acetyl-beta-D-glucosaminidase activity in residual milk was significantly lower than in foremilk from PIH 4 to 24 and from PIH 24 to 59, respectively. Regarding total and differential leukocyte counts, values for the 2 fractions followed the same pattern throughout the course of inflammation, probably owing to frequent sample collection. Total and differential cell counts tended to differ between the fractions during some periods, although differences were not statistically significant. When samples were taken less frequently, the total leukocyte concentration in residual milk was higher than that in foremilk. Although sample collections were frequent, clustering of immature neutrophils was not observed in the cytofluorogram of blood leukocytes in this study. Residual milk seems to be the fraction that best reflects the condition in the quarter at the particular time when the milk sample is taken. Results also indicate that residual milk reflects the condition of the secretory tissue, as well as the lower regions of the gland.