The objective of Exp. 1 was to compare the effects of virginiamycin (VM; 0, 175, or 250 mg x animal(-1) x d(-1)) and monensin/tylosin (MT; 250/ 90 mg x animal(-1) x d(-1)) on ruminal fermentation products and microbial populations in cattle during adaptation to an all-concentrate diet. Four ruminally cannulated, Holstein steers were used in a 4x4 Williams square design with 21-d periods. Steers were stepped up to an all-concentrate diet fed at 2.5% of BW once daily. Ruminal pH, protozoal counts, and NH3-N and VFA concentrations generally were unaffected by VM or MT. Mean counts of Lactobacillus and Streptococcus bovis were lower (P<.05) for VM-treated compared with control or MT-treated steers. Both VM and MT prevented the increase in Fusobacterium necrophorum counts associated with increasing intake of the high-concentrate diet observed in the control. The objective of Exp. 2 was to compare the effects of VM and MT on ruminal pH, L(+) lactate and VFA concentrations, and F. necrophorum numbers during carbohydrate overload. Six ruminally cannulated Holstein steers were assigned randomly to either the control, VM (175 mg/d), or MT (250 + 90 mg/d) treatments. Acidosis was induced with intraruminal administration of a slurry of ground corn and corn starch. The VM and MT premixes were added directly to the slurry before administration. Carbohydrate challenge induced acute ruminal acidosis (pH was 4.36 and L (+) lactate was 19.4 mM) in controls by 36 h. Compared with the controls, steers receiving VM or MT had higher (P<.05) ruminal pH, and the VM group had a lower (P<.05) L (+) lactate concentration. Fusobacterium necrophorum numbers initially increased in VM- and MT-administered steers. In the control steers, F. necrophorum was undetectable by 36 h. Virginiamycin seemed to control the growth of ruminal lactic acid-producing bacteria and, therefore, has the potential to moderate ruminal fermentation in situations that could lead to rapid production of lactic acid.

Twelve ruminally cannulated Holstein steers were used to determine the effect of monensin (0, 20, 30, and 40 g/ton) on grain bloat. Steers were fed a bloat-provocative, high-grain diet at 1% of body weight twice daily. Monensin premix was added directly to individual steers diets at the time of feeding. The severity of bloat was scored daily on a scale of 0 (no bloat) to 5 (severe bloat). The scoring was based on the degree of frothiness and abdominal distention. Bloat scores (mean of wk 2, 3, and 4) were lower (P<.0l) for monensin-fed steers than for the controls. The mean bloat scores were 1.43, 1.18, 1.00, and .93 for 0, 20, 30 and 40 g/ton monensin, respectively. Total gas production during in vitro ruminal fermentation tended to be higher (P=.12) for control than for monensin-fed steers. Ruminal pH and total volatile fatty acid concentrations were unaffected by treatment. Monensin decreased frothy bloat caused by the bloat-provocative diet, and the degree of control appeared to be greater with higher levels of monensin. Twelve ruminally cannulated Holstein steers were used to determine the effect of monensin (0, 20, 30, and 40 g/ton) on grain bloat. Steers were fed a bloat-provocative, high-grain diet at 1% of body weight twice daily. Monensin premix was added directly to individual steers diets at the time of feeding. The severity of bloat was scored daily on a scale of 0 (no bloat) to 5 (severe bloat). The scoring was based on the degree of frothiness and abdominal distention. Bloat scores (mean of wk 2, 3, and 4) were lower (P<.0l) for monensin-fed steers than for the controls. The mean bloat scores were 1.43, 1.18, 1.00, and .93 for 0, 20, 30 and 40 g/ton monensin, respectively. Total gas production during in vitro ruminal fermentation tended to be higher (P=.12) for control than for monensin-fed steers. Ruminal pH and total volatile fatty acid concentrations were unaffected by treatment. Monensin decreased frothy bloat caused by the bloatprovocative diet, and the degree of control appeared to be greater with higher levels of monensin.

The goal of this paper is to briefly review calcium homeostasis, to present four methods of prevention of milk fever and to discuss advantages, disadvantages and mode of action of each method.