Lasalocid or monensin inhibited most of the lactate-producing rumen bacteria (Butyrivibrio fibrisolvens, Eubacterium cellulosolvens, E. ruminantium, Lachnospira multiparus, Lactobacillus ruminis, L. vitulinus, Ruminococcus albus, R. flavefaciens, Streptococcus bovis). Minimum inhibitory concentrations ranged from .38 to 3.0 micrograms/ml. Among the lactate producers, those that produce succinate as a major end product (Bacteroides, Selenomonas, Succinimonas, Succinivibrio) were not inhibited by lasalocid or monensin. Also, none of the major lactate fermenters (Anaerovibrio, Megasphaera, Selenomonas) was inhibited by lasalocid or monensin. Veillonella alcalescens was inhibited by 24 micrograms/ml of lasalocid but was resistant to monensin. Hence, the reported increase in propionate in lasalocid- or monensin-fed cattle may result from selection for succinate producers and lactate fermenters. Lasalocid and monensin appeared to inhibit selectively the production of L(+), but not D(-) lactic acid. The inhibition of major lactate-producing bacteria (Streptococcus and Lactobacillus) suggests that lasalocid or monensin may be used to prevent lactic acidosis in ruminants.

Lasalocid, monensin or thiopeptin was administered intraruminally each at .33, .65 or 1.3 mg/kg body weight and evaluated for its effectiveness in preventing experimentally induced lactic acidosis in cattle. Four rumen-fistulated cattle were used for each dosage level and the design was a 4 x 4 Latin square with each animal receiving lasalocid, monensin, thiopeptin or no antibiotic. Acidosis was induced by intraruminal administration of glucose (12.5 g/kg body weight). Control cattle exhibited the typical drop in rumen pH and concurrent increases in L(+) and D(-) lactate concentrations commonly observed in cases of lactic acidosis. Alkali reserves were depleted in the control cattle as evidenced by a decrease in blood bicarbonate and a negative shift in base excess. In all three trials, cattle given lasalocid had higher rumen pH and lower lactate concentrations than did control cattle or cattle given monensin or thiopeptin. Cattle given monensin had a significantly higher rumen pH and a lower lactate concentration than the controls only at the .65 and 1.3 mg/kg body weight dosages, whereas thiopeptin was effective only at the 1.3-mg dosage. Concentrations of total VFA in rumen fluid decreased in the controls but remained unchanged in cattle given antibiotics. A significant reduction in the molar proportion of acetate and an increase in the molar proportion of propionate were observed in the rumen fluid of the cattle given antibiotics. Colony counts of Streptococcus bovis and Lactobacillus were significantly reduced in rumen fluid of cattle given 1.3 mg antibiotic/kg body weight. Counts of lactate-utilizing bacteria increased in both control cattle and cattle given antibiotics. Cattle given antibiotics showed no evidence of lacticacidemia, hemoconcentration or change in acid-base balance.

Intraruminal administration of lasalocid or monensin (1.3 mg/kg body weight) effectively prevented in glucose- or corn-induced lactic acidosis in cattle. Administering the antibiotics for 7 days before experimentally inducing acidosis with corn (27.5 g/kg body weight), effectively prevented acidosis, while 2 days' were sufficient to prevent glucose-induced acidosis (12.5 g/kg body weight). The different responses observed in the two trials probably stemmed from the difference in amounts of carbohydrate used to induce acidosis. Antibiotic-treated cattle had higher rumen pH values and lower L(+) and D(-) lactate concentrations that control cattle that received no antibiotics. Ruminal VFA in control cattle decreased, while total VFA and the molar proportion of propionate increased in antibiotic-treated cattle after grain engorgement. Control cattle exhibited classic signs of acidosis, such as lowered blood pH; increased blood lactate, particularly D(-) isomer; hemoconcentration, and depleted alkali reserve with a pronounced based deficit. Antibiotic-treated cattle exhibited no signs of systemic acidosis.

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Feeding grain to animals not adapted to grain resulted in a marked increase in the ./. concentration of free endotoxln m the rumen. Endotoxin concentration increased 15 to 18 times within 12 hr after lactic acidosis was induced through grain engorgement. The increase was accompanied by a shift from predominantly gram-negative to gram-positive bacteria. Data from in vitro fermentations showed that the increase in free endotoxin concentration was not accompanied by a decrease in the number of gram-negative bacteria. The absorption of endotoxin from the rumen was not apparent by the actinomycin D assay procedure because no difference was observed in mice lethality of plasma from control and post-engorgement samples. However, the significant granulocytosis that accompanied acidosis was suggestive of systemic action of rumen bacterial endotoxin.

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Two rumen-fistulated Holstein heifers were fed three protein-free semipurified diets: 70% roughage, 30% concentrate; 50% roughage, 50% concentrate; and 30% roughage, 70% concentrate. Wheat straw was the roughage, and the concentrate was a pelleted mixture of corn starch, dextrose, fat, urea, vitamins, and minerals. Each animal received the three dietary treatments in a randomized complete block design. On days 1, 3, and 5 following a 21-day adaptation, rumen fluid samples were taken before feeding and at 1, 2, 3, 4, and 5 h after feeding. Total protozoa concentrations for low, medium, and high concentrate diets were 1.5, 2.5, 4.1 X 10(5)/ml. Dasytricha concentrations were not affected by diet, but Entodinium, Diplodinium, Isotricha, Epidinium, and Ophryoscolex increased with increases of the concentrate proportion of the diets. Entodinium, the predominant protozoa with all diets, increased as concentrate proportion of the diet increased. In a second experiment the two heifers from Experiment 1 were fed semipurified diets that contained either urea or soybean meal as the nitrogen source. There were larger populations of Dasytricha and Isotricha when the diet contained soybean meal, and larger populations of Charon, Entodinium, and total protozoa when the diet contained urea. In both experiments, holotrichs were highest 1 to 2 h after feeding, and entodiniomorphs were highest before feeding and 4 to 6 h after feeding. An active protozoan population can exist in the rumen of cattle fed diets virtually devoid of natural protein, and protozoa are influenced by energy and nitrogen source.