Two Holstein cows were fed Rumensin for 12 weeks, beginning approximately 90 days postpartum. Milk production increased 7%, whereas percentage fat in milk decreased 10.3%. Percentage protein in milk increased 9.6% in the early stages and decreased 10.2% in the late stages of the study. Daily fat yield did not change, whereas protein yield increased in the early stages, but did not change in later stages. Fat corrected milk (FCM) did not change with treatment, but dry matter intake (DMI) tended to increase when Rumensin was fed. Acetate concentration did not change whereas propionate concentration increased, causing a significant decrease in ruminal acetate:propionate ratio. Rumen pH showed a nonsignificant numerical increase.; Dairy Day, 1987, Kansas State University, Manhattan, KS, 1987
Four rumen-fistulated steers, randomly assigned to two groups (control and salinomycin fed) were used to monitor the changes in rumen microbial populations and volatile fatty acids (VFA) concentrations associated with feeding salinomycin (0.22 mg X kg-1 X day-1). Steers were adapted to an alfalfa hay and grain (80:20) diet before supplementing the diet with salinomycin, and then the diet was changed to 50:50 and 20:80 ratios of alfalfa hay to grain at 2-week intervals. Rumen samples for total and selective enumeration of anaerobic bacteria. VFA analysis, and enumeration of protozoa were collected during the 80:20 alfalfa hay-to-grain diet before salinomycin feeding, and during the 80:20, 50:50, and 20:80 hay-to-grain diets with salinomycin. At each sampling period, rumen samples were collected at 3 h after feeding on three consecutive days. Salinomycin feeding had no effect on rumen pH and total VFA concentration. The acetate-to-propionate ratio was significantly lower in salinomycin-fed steers than in the control. The molar proportion of butyrate increased in both control and salinomycin-fed steers. Total anaerobic bacterial counts were lower in salinomycin-fed steers than in the control steers after 8 weeks of salinomycin feeding. Salinomycin-resistant bacteria increased from 7.6 to 15.6% in salinomycin-fed steers but remained unchanged in control steers. Salinomycin had no effect on cellulolytic and lactate-utilizing bacteria, but the proportion of amylolytic bacteria was higher in salinomycin-fed steers than in control steers. The total number of protozoa decreased initially in salinomycin-fed steers. The initial reduction was due to reduced numbers of Entodinium species. Holotrichs were unaffected by salinomycin feeding.
The sudden death syndrome (SDS) is a relatively new problem in the feedlot industry. With SDS, apparently healthy cattle in late finishing die suddenly with no sign of sickness or lesions indicative of other diseases. Rumen fluid pH, histamine, total lactate, L(+) lactate and volatile fatty acids (VFA) were compared among 19 SDS cattle, two animals with lactic acidosis produced through grain engorgement, and six healthy feedlot cattle maintained on a high energy finishing ration more than 100 days. Rumen fluid from the lactic acidotic cattle was high in lactic acid and histamine concentrations, low in pH, and low in total volatile fatty acid (VFA) concentration. The rumen fluid from feedlot steers used as controls had moderately high total VFA concentrations, narrow acetate-to-propionate ratios, low lactic acid concentrations, no histamine, and pH below 6. Concentrations of lactic acid, histamine, and total VFA varied in rumen fluid from SDS cattle. There was no relationship between SDS and rumen pH, or the concentrations of histamine, lactic acid or total VFA.
Thirty-two Holstein heifer calves receiving conventional rations were supplemented with 0 (control), 125, 250, or 500 IU vitamin E/calf/day. The objective was to determine the optimum requirement based on their performance from birth to 24 wk of age. Results on weight gains, feed consumption, serum enzymes indicative of cell membrane damage, immune responses, and metabolic profile indicated that supplementation of calves receiving conventional rations with 125 to 250 IU/day may maximize their performance.; Dairy Day, 1986, Kansas State University, Manhattan, KS, 1986
Two rumen fistulated cows, not adapted to urea, were given .5 g urea intraruminally per 1 kg body weight 16 hr after a previous feeding. Ammonia-N concentration 5 min after dosing rose from .13 to .71 mg per 100 ml for carotid blood and from .11 to .43 mg for jugular blood, then to 1.47 mg (carotid) and .95 mg (jugular) at time of toxicity. Toxicity, judged by appearance of definite muscle tetany, occurred between 17 and 30 min after dosing. The marked difference in ammonia concentrations in carotid and jugular blood suggests that the brain takes up ammonia rapidly. Other changes observed between dosing and toxicity were: rumen ammonia-N, 6.18 to 51.30 mg per 100 ml; rumen pH, 6.94 to 7.90; arterial blood pH, 7.44 to 7.50; arterial blood pO2 , 87.1 to 96.1; blood lactic acid, 9.5 to 23.4 mg per 100 ml; blood glucose, 72 to 91.9 mg per 100 ml; and packed cell volume, 24.5 to 28.5%. Plasma protein did not change. Heart beat increased slightly to toxicity (63.8 to 71.8 beats per minute) and more markedly after toxicity. No significant changes in electrocardiographic patterns were observed. Emptying the rumens at toxicity resulted in complete recovery within 1 hour.
D-penicillamine has been used in the treatment of rheumatoid arthritis for years. As a rare complication of this treatment the occurrence of myasthenia gravis has been described, the clinical features of this complication being indistinguishable from that of idiopathic myasthenia gravis. Both D-penicillamine induced and idiopathic myasthenia gravis show elevated titers of acetylcholine receptor antibodies and respond to acetylcholinesterase inhibitor treatment. We report on a patient with rheumatoid arthritis who, under treatment with D-penicillamine, developed severe myasthenia gravis which required temporary acetylcholinesterase inhibitor therapy. 8 months after D-penicillamine was discontinued the acetylcholine receptor antibodies had disappeared and the acetylcholinesterase inhibitors could be withdrawn. Clinical findings and possible pathogenetic aspects of D-penicillamine induced myasthenia gravis are discussed.
Two Holstein heifers and a steer fitted with ruminal and duodenal cannulas were used to determine acid-base and electrolyte changes associated with metabolic alkalosis induced by duodenal obstruction. Obstruction was induced distally to the pylorus, but proximally to the common bile duct entrance. Ruminal fluid, blood, and urine samples were obtained before and after obstruction was induced. Duodenal obstruction resulted in increased blood pH, bicarbonate concentration, and base-excess values. Severe hypochloremia and hypokalemia were evident in 48 hours. Serum sodium concentration decreased only slightly. Packed cell volume and serum concentrations of urea nitrogen, creatinine, glucose, and inorganic phosphate increased, whereas calcium concentration showed no change. Renal chloride excretion reached near zero in 24 hours, whereas sodium and potassium excretions decreased in the steer, but were unchanged in the heifers. Urine creatinine concentration increased markedly in the heifers and steers. Acid urine was not evident up to 96 hours. Ruminal fluid pH decreased and chloride concentration increased in the steer, but remained unaffected in the heifers. Duodenal obstruction had no effect on rumen sodium, calcium, and magnesium concentrations, but the potassium concentration increased in the heifers. The degrees of alkalosis and electrolyte changes were greater in the steer than in the heifers.
