Objectives of this field investigation were to examine the etiology and mastitis infection dynamics in a 60 cow herd in danger of market loss, prioritize and implement prevention strategies, and evaluate the efficacy of recommended and extended therapy (S. aureus only) with pirlimycin hydrochloride (Pirsue, Pfizer Animal Health) for gram positive intramammary infections (IMI) . Initial percentages (October) of cows (quarters) uninfected or infected with Staph. aureus, Strep. dysgalactiae, alpha hemolytic strep., and Strep. uberis, were 42(65); 33(15%); 20(9); 3(1); and 2(0.4), respectively. Overall streptococci cure rates were 91% and 89% of cows and quarters, respectively and was higher than average published values (65-70%). Cure rates for Staph. aureus (extended pirlimycin therapy) were very low at 7% and 4% of cows and quarters, respectively. Overall results showed excellent therapy response for Strep. IMI but very low S. aureus cure rates. However, some therapy success coupled with critical and mandatory prevention strategies (including a strict milking order) resulted in a 50% decrease in SCC by January and limited new infections. Failure to continue these proper prevention strategies resulted in many new IMI and high herd SCC in February, and demonstrates the mandatory requirements for proper mastitis prevention strategies (including a milking order) in a comprehensive mastitis and milk quality program.

Forty multiparous Holstein cows were assigned to a 2×2 factorial arrangement of treatments to compare heat-treated soybean meal and heat-treated whole soybeans as protein supplements and to measure the effects of 6g of supplemental niacin/d. Treatments began 10 d prior to calving and continued through 15 wk postpartum. Dry matter intake was .9 kg/d more for cows fed heat-treated soybean meal than for those fed heat-treated soybeans. The latter diet contained about 2.5% more lipid, resulting in similar daily energy intakes of 34.3 and 33.6 Mcal NE1 for heat-treated soybean meal and heat-treated soybean diets. Niacin tended to improve DM intake of cows fed diets containing heat-treated soybeans.

Cows (n = 139) were sampled within 17 d postpartum and monthly thereafter to examine dynamics of mammary infections and relationships between infection status, milk yield, SCC, NAGase activity, and chloride concentration. Forty-eight and 67% of cows and 19.5 and 30.5% of quarters were infected at first test and lactation end, respectively, with 51% of all infections present at first test. Coagulase-negative staphylococci accounted for 67 and 65% of first test and total infections with 85% persisting to lactation end. Animals with coagulase-negative staphylococci infections had significantly elevated quarter SCC and NAGase activity and a decrease of 821 kg mature equivalent lactation milk production compared with uninfected animals. Clinical cases with no bacterial isolation or major pathogen infections were associated with significant elevations in bucket and quarter milk SCC, NAGase activity, chloride concentration in quarters, and a decrease of 1153 kg mature equivalent lactation milk production as compared with uninfected animals. Correlations between milk production and in SCC and ln NAGase and between ln SCC and ln NAGase were -.15, -.25, and .55 (-.23, -.28, and .41 for first lactation only).

Effects of sterile intramammary infusion of Concanavalin A on milk secretion were contrasted with infusion of oyster glycogen or water. Twenty-four cows were infused intramammary with 100 mg Concanavalin A, oyster glycogen in 20 ml water, or with 20 ml water alone. Concentrations of lactose, somatic cells, immunoglobulins G and A, serum albumin, and activity of N-acetyl-B-D-glucosaminidase were determined in milk. Blood N-acetyl-B-D-glucosaminidase activity and concentrations of blood immunoglobulins G and A and serum albumin were determined. Oyster glycogen and concanavalin A caused inflammation in treated quarters; peak elevations of milk somatic cell counts, serum albumin, immunoglobulin G concentrations, and N-acetyl-B-D-glucosaminidase activity were at 12 to 36 h following treatment. Milk production and lactose concentration were reduced by oyster glycogen and Concanavalin A. Selective indices of relative accumulation of milk immunoglobulins decreased following Concanavalin A and oyster glycogen, whereas the N-acetyl-B-D-glucosaminidase activity selective index generally remained unchanged. Inflammation reduced the selective accumulation of immunoglobulins, and absence of change in the N-acetyl-B-D-glucosaminidase selective index indicated that blood is not a major source of milk N-acetyl-B-D-glucosaminidase.

Twenty-six cows that developed positive milk tests for ketosis in early lactation were randomly assigned to one of three groups: 1) control, 2) propylene glycol (125 ml/d), or 3) 125ml of propylene glycol plus 12g of niacin daily. Treatments were administered for 7 d. Changes in milk production, milk composition, and feed intake were similar for all three groups. None of the cows in any of the groups developed clinical ketosis. During the 14-d monitoring period from the start of treatment there were similar increases in blood glucose in all groups. Declines in plasma beta-hydroxybutyrate and free fatty acids over the period were also similar for all treatments. Results reinforce the concept that optimum feeding and management reduces the need for additives for ketosis control.

Information on milking rate, monthly bucket somatic cell counts, mastitis treatment, and milk production was obtained from 284 lactations of Holstein cows separated into three lactation groups. Significant correlations between somatic cell count (linear score) and other parameters included production in lactation 1 (-.185), production in lactation 2 (-.267), and percent 2-min milk in lactation 2 (.251). Somatic cell count tended to increase with maximum milking rate in all lactations, but correlations were not statistically significant. Twenty-nine percent of cows with milking rate measurements were treated for clinical mastitis. Treated cows in each lactation group produced less milk than untreated cows. In the second and third lactation groups, treated cows had a shorter total milking time and a higher percent 2-min milk than untreated cows, but differences were not statistically significant. Overall, the data support the concept that faster milking cows tend to have higher cell counts and more mastitis treatments, particularly beyond first lactation. However, the magnitude of the relationship was small.

Milk and plasma N-acetyl-B-D-glucosaminidase activity was determined for cows during the dry and early postpartum periods. Milk samples were taken from individual quarters of 12 cows from 7 d preceding dry off until calving. Weigh jar milk samples were taken daily for 28 d postpartum from 9 of the 12 cows. Somatic cell concentration was also measured in the postpartum samples. N-Acetyl-B-D-glucosaminidase activity of mammary secretions was significantly elevated in the dry period. Activity in mammary secretions was significantly higher than blood plasma concentrations during the dry period, which suggests that the enzyme present in mammary secretions comes mainly from within the gland. Milk enzyme concentrations declined sharply by 4 d postpartum and gradually declined through 28 d postpartum. Activity was still slightly elevated at 28 d postpartum as compared with normal lactation. Greater daily variability was seen with somatic cells than with N-acetyl-B-D-glucosaminidase. However, somatic cells were more responsive to clinical infections postpartum, showing significant elevations in both clinical episodes. The enzyme was elevated in one clinical case, but relatively unchanged in the other. Plasma levels were constant throughout both trials.

Fifty-eight multiparous cows were assigned randomly to one of two rations. Control cows received a concentrate mixture that contained 20% soybean meal as the protein supplement, and the experimental cows were fed a concentrate that contained 25% heat-treated whole soybeans. The experimental period started 10 d after calving and continued for 15 wk.

N-Acetyl-B-D-glucosaminidase activity, somatic cell count, and udder infection status were determined in milk of nine Saanen goats. Plasma enzyme activity was also measured. Individual half udder milk samples were taken for 12 d over a 3-wk period and animals were bled weekly. Three of the 18 udder halves were infected with coagulase-negative staphylococci over all 12 sampling d. The N-acetyl-B-D-glucosaminidase and somatic cells in milk were significantly elevated in samples where minor pathogens were isolated. Plasma enzyme was variable among goats but not within goats or across weeks. Greater daily variation was seen in somatic cell count as compared to milk enzyme activity. Correlation between milk N-acetyl-B-D-glucosaminidase and somatic cell count was .54.

Sixteen cows in middle to late lactation were milked for 3.5 days at 12-h intervals except for a 24-h interval between third and fourth milkings. A cowside quarter milking unit was used. Quarters were classified by infection status. Milk chloride, lactose, somatic cell concentrations, N-acetyl-B-D-glucosaminidase activity, and cell differential counts were determined. Following the omitted milking, concentrations of milk chloride and somatic cells were elevated and lactose concentration reduced in infected quarters. In uninfected quarters, chloride concentration increased, and lactose concentration decreased after the 24-h interval. The milk N-acetyl-B-D-glucosaminidase activity was elevated only in quarters infected with major pathogens. Changes of milk secretion induced by an omitted milking are affected by infection status, and additional secretory cell damage in quarters infected with a major pathogen may result from an omitted milking.

Relationship between milk production and milk composition was studied through comparisons of udder halves within cow. Cows were milked by milking unit for separate quarters of udder. Six trials had six cows per trial. Trial length was 3 d, and milkings were at 12-h intervals. Foremilk samples were taken aseptically for bacterial analysis. Milk weights by quarter were recorded, and samples by quarter were analyzed for concentrations of lactose, somatic cells, and chloride. Milk cell differential counts and N-acetyl-B-D-glucosaminidase activity also were determined. Eighty-four percent of quarter milk samples contained less than 400,000 cells/ml. Differences between right and left udder halves with respect to all measurements were computed. For halves of udders within-cow correlation coefficients for differences between production and log(base 2) somatic cell count, lactose, chloride, bacterial presence, neutrophil percent, lymphocyte percent, macrophage percent, and N-acetyl-B-D-glucosaminidase activity were -.16, .23, -.31, .09, .12, .01, -.14, and -.41. Regression coefficients of milk production (kg) on somatic cell count log(base 2) cells per milliliter, lactose (%), chloride (mg/100 ml), and N-acetyl-B-D-glucosaminidase (nmol/min per ml) were -.12, .57, -.05, and -.46. From negative correlations between production and concentrations of chloride, somatic cells, and N-acetyl-B-D-glucosaminidase activity, differences between udder halves in production may be related to changes of the blood-milk barrier, leukocyte diapedesis, and loss of integrity of secretory cells.

Intramammary treatment with a broad spectrum antibiotic was evaluated for cows treated after a single high monthly somatic cell count or for cows with clinical mastitis. Forty-three quarters of 36 cows were treated after a high somatic cell count, and 56 quarters of 48 cows were treated after clinical symptoms.

Bulk tank milk samples collected from 175 dairy herds throughout Wisconsin averaged 466 micrograms of iodine per liter with 11% of the samples containing greater than 1000 micrograms per liter. From questionnaires on feeding and management, use of iodine supplements in feed was associated with increased iodine in milk. One gram of ethylenediamine dihydriodide was fed daily for 2 wk to dairy cows with a history of mastitis. Milk iodine increased from 210 to 6225 micrograms per liter. There was no significant effect on somatic cells, mastitis organisms, or incidence of clinical mastitis.

In two trials with 44 cows over an 8-wk dry period, control cows were fed alfalfa forage and minimal grain compared to liberal grain plus corn silage (Trial 1) or plus alfalfa forage (Trial 2). Following parturition all cows were fed to meet requirements. In trial 2 half of each group received nicotinic acid at approximately 12g daily for 8 wk, starting on the 8th day postpartum.

In feeding trials to clarify the mechanism by which unsaturated oils depress milk fat percentage, oleic acid at 250 or 500 ml per cow per day did not reduce milk fat percentage significantly. At 500 ml these changes were significant (control, oleic): rumen acetate 61.6, 60.3%; rumen propionate 19.4, 21.0%; milk fat content of 18:1 trans fatty acid 3.0, 8.0%; and of 18:2 cis fatty acid 2.2, 1.4%. Feeding hydrogenated vegetable oil containing 13% trans acid at 454 g per cow per day decreased slightly milk fat percentage and elevated plasma cholesterol 190 to 245 mg/100 ml and 18:1 trans fatty acid in milk fat 4.2 to 6.2%. Hydrogenated vegetable oil containing 49% 18:1 trans acid at 454 g daily decreased milk fat 3.9 to 3.1%. Milk fat triglycerides decreased in short chain fatty acids and increased in 18:1 trans 2.6 to 11.2%, 18:1 cis 22.9 to 29.0%, and 18:2 trans .2 to 1.8%. Milk phospholipids decreased 14.1 to 9.6% in 14:0 fatty acid and increased .3 to 3.1% in 18:1 trans and 20.5 to 31.4% in 18:1 cis. Blood cholesterol esters were increased 152 to 195 mg/100 ml. The data lend support to the concept that trans acids or compounds produced in the rumen during their formation from polyunsaturated fatty acids are responsible for the milk fat depression from unsaturated oils.

Effects of nicotinic acid on glucose metabolism were studied in a series of experiments with goats.Oral administration of single doses of nicotinic acid (6.5 to 17.0 g) elevated blood glucose, impaired glucose tolerance, and elevated insulin.The magnitude of the effects was related positively to nicotinic acid dosage.Maximum effect occurred 2 to 3 days after administration.Blood glucose was elevated, with or without glucose administration, despite markedly elevated insulin.However, exogenous insulin given 48 h after nicotinic acid still reduced blood glucose although the response was delayed and was less than in control animals.A lactating cow given 160 g nicotinic acid exhibited alterations in glucose metabolism similar to control animals.These studies demonstrate that nicotinic acid, in addition to previously reported effects on lipid metabolism, also has significant effects on carbohydrate metabolism.

Changes in blood metabolites and milk production were measured in eight cows with subclinical or clinical ketosis following treatment with daily doses of 12 g nicotinic acid fed with the concentrate mixture. Ketotic cows displayed a positive milk ketone test, reduced milk production and feed intake, hypoglycemia, hyperketonemia, and elevated free fatty acids in plasma. The milk ketone test was negative in all cows 5 to 9 days following initiation of treatment. After 7 days of treatment, milk production and glucose in plasma were increased while there were decreases in plasma beta-hydroxybutyrate and free fatty acids. No relapses occurred.