Reference

Monensin toxicosis in swine: potentiation by tiamulin administration and ameliorative effect of treatment with selenium and/or vitamin E

Monensin toxicosis in swine: potentiation by tiamulin administration and ameliorative effect of treatment with selenium and/or vitamin E. Van Vleet, John F.; Runnels, Lewis J.; Cook, James R., Jr.; Scheidt, Alan B. (Sch. Vet. Med., Purdue Univ., West Lafayette, IN 47907, USA). Am. J. Vet. Res., 48(10), 1520-4 (English) 1987. CODEN: AJVRAH. ISSN: 0002-9645. DOCUMENT TYPE: Journal CA Section: 1 (Pharmacology) Section cross-reference(s): 18 Prominent acute clin. signs of monensin toxicosis (hypermetria, hind limb ataxia, paresis, knuckling of hind limbs, and recumbency) developed by 2 to 6 h after dosing in pigs given 15 or 25 mg of monensin/kg with tiamulin exposure, but not in pigs given the 15 or 25 mg of monensin/kg without tiamulin exposure. Also, the extent of monensin-induced skeletal muscle damage at 4 days after monensin dosing was enhanced in pigs given 7.5, 15, or 25 mg of monensin/kg and exposed to tiamulin. Treatment of pigs with Se-vitamin E or with vitamin E only prior to monensin administration gave protection against monensin-induced skeletal muscle damage and indicated that vitamin E, rather than Se, was essential to provide this protection. However, treatments with Se-vitamin E, Se, or vitamin E did not alter the severity of acute clin. signs of monensin toxicosis. In swine, different pathogenetic mechanisms may be responsible for early transient clin. signs of monensin toxicosis and for the late-appearing lesions of skeletal muscle damage.

Relative contributions of ruminal bacteria and protozoa to the degradation of protein in vitro

Relative contributions of ruminal bacteria and protozoa to the degradation of protein in vitro. Hino, Tsuneo; Russell, James B. (Dep. Anim. Sci., Cornell Univ., Ithaca, NY 14853, USA). J. Anim. Sci., 64(1), 261-70 (English) 1987. CODEN: JANSAG. ISSN: 0021-8812. DOCUMENT TYPE: Journal CA Section: 18 (Animal Nutrition) Section cross-reference(s): 10 Mixed ruminal microorganisms from a cow fed timothy hay and conc. supplement () were incubated with various protein sources for 15 h (no carbohydrates), and deamination was studied under enzyme-limiting substrate-excess conditions. Addn. of amphotericin [12633-72-6] (10 mg/mL) killed protozoa and decreased ammonia prodn. from killed bacteria but it had no effect on casein deamination. Monensin [17090-79-8] (5 mg/mL) also killed protozoa; however, it decreased casein deamination to a much greater extent than amphotericin. Antibacterial antibiotics (penicillin G [61-33-6], polymixin B [1404-26-8], cephalosporin C [61-24-5] and streptomycin [57-92-1]) greatly reduced ammonia formation from casein. Isolated bacteria always produced more ammonia than isolated protozoa, but the difference was less with heat-treated, particulate proteins. Heated soybean protein was as sol. as heated casein but it was deaminated at a faster rate by bacteria. Nonammonia-nonprotein N accumulation was greater with the protozoa than bacteria. When incubations contg. bacteria or protozoa were compared with combinations of protozoa and bacteria, the combinations always caused a synergistic increase in ammonia and decrease in nonammonia-nonprotein N. These results suggest: 1) sol. proteins were primarily degraded by bacteria; 2) protozoa could contribute to the degrdn. of insol., particulate proteins; 3) protozoa were limited in their ability to assimilate peptides (or amino acids); 4) low mol. wt. products could be fermented more readily by bacteria and 5) monensin was toxic to protozoa, but decreases in ammonia were primarily due to action of monensin on bacteria.