An 8-wk growth trial was conducted to assess the effects of ovine growth hormone (oGH; 7 mg/d, sc) on growth performance and carcass composition of normal, growing wether lambs. Diethylstilbestrol (DES; .1 mg/d, sc) and control lambs were included for comparisons. Plasma oGH levels at 8 wk were 1.9, 5.5 (P less than .05) and 138.1 ng/ml (P less than .001) for controls, DES and oGH lambs, respectively. Diethylstilbestrol did not increase plasma oGH until the fourth week. The oGH improved feed conversion 7.4% (FC; P less than .05), but did not alter average daily gain (ADG) or feed intake (ADF). Diethylstilbestrol increased ADG 15.3% (P less than .05) and improved FC 16.1% (P less than .01), with no effect on ADF. The primary effect of oGH on carcass composition was to decrease the quantity of fat 8.9% (P less than .05). In addition, oGH may have increased protein 6.5% (P less than .10) and moisture 4.0% (not significant). Diethylstilbestrol increased the quantity of carcass protein 10% (P less than .01) and moisture 8.7% (P less than .05), with no effect on fat. In these studies, the primary effect of exogenous oGH on normal, growing lambs was to reduce carcass fat, which may account for the observed improvement in FC. Diethylstilbestrol, at 1/70th of the oGH dose, was superior to oGH for improving FC (P less than .05) and ADG (P less than .10). Improvements in body weight of the lambs given DES were observed 2 wk before an increase in plasma oGH. In addition, DES, unlike exogenous oGH, did not alter the quantity of carcass fat. These observations do not support the concept that the mode of action of DES is through increased GH secretion.

Thiopeptin, thiopeptin-like antibiotics and penicillin were shown previously to be highly active in vitro against Streptococcus bovis, the microorganism believed to be responsible for the initiation of ruminal lactic acidosis. The purpose of this work was to determine the efficacy of these antibiotics in preventing lactic acidosis in lambs challenged by intraruminal administration of ground wheat. Lambs, which were fasted and then given ground wheat at 40 g/kg body weight, showed dramatic increases in rumen and plasma lactate over the 30-hr experimental period. Rumen lactate increased from .2 to peak levels of approximately 150 mumoles/ml by 8 to 10 hr after wheat administration. Plasma lactate increased after rumen lactate was elevated and lambs succumbed when plasma levels exceeded 15 mumoles/ml. Ruminal volatile fatty acids were greatly reduced as rumen lactate increased. Over half of the lambs given ground wheat died within 30 hours. Thiopeptin given as a single dose completely prevented lactic acidosis by reducing rumen lactate 80 to 90%. In addition, thiopeptin permitted "normal" rumen fermentation to continue as indicated by a significant increase in volatile fatty acids. The minimum effective dose of thiopeptin to control acute lactic acidosis was .18 mg/kg body weight. Other members of the thiopeptin class, including sulfomycin, sporangiomycin, siomycin and taitomycin, prevented lactic acidosis in a manner similar to thiopeptin. Penicillin, however, inhibited ruminal volatile fatty acid production as well as lactate synthesis. In addition, the effective period for penicillin in the rumen was only 8 to 16 hr, after which lactate fermentation was reestablished. Thus, thiopeptin and thiopeptin-like antibiotics, but not penicillin, appear to provide prophylactic treatment against lactic acidosis in sheep.

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