|KRAUSE, DENIS - CORNELL UNIVERSITY
Submitted to: Applied and Environmental Microbiology
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 12/15/1995
Publication Date: N/A
Interpretive Summary: Ruminal amino acid deaminationis a nutritionally wasteful process that increases the urea excretion of ruminants. Previously isolated ruminal bacteria could not explain the ammonia production of ruminal bacteria in vivo, but recently isolated obligate amino acid-fermenting ruminal bacteria had 20-fold higher rates of deamination. The antibiotic monensin is routinely fed to ruminants, but its ability to spare amino acids was largely ignored. An in vitro continuous culture system indicated that monensin was only inhibiting two of the three amino acid-fermenting bacteria. Clostridium aminophilum persisted in continuous culture, and similar results were observed in vivo. Since C. aminophilum is not readily inhibited by monensin, other inhibitors with greater activity towards C. aminophilum will be needed to provide even greater degrees of amino acid- sparing. The inhibition of amino acid deamination will decrease the cost of ruminant production and decrease environmental pollution.
Technical Abstract: Predominant ruminal bacteria (PRB) that were isolated from a 10 8 dilution of ruminal fluid could not utilize peptides or amino acids as an energy source for growth. rRNA from PRB did not hybridize with the probes to obligate amino acid-fermenting ruminal bacteria, Peptostreptococcus anaerobius (C), Clostridium sticklandii (SR) and a new species designated as Clostridium aminophilum F. When the PRB were grown in continuous culture with carbohydrates and increasing amounts of Trypticase, the steady state concentration of ammonia in the culture vessel increased, but only a small fraction of the Trypticase was deaminated. The ionophore monensin had little effect on the ammonia production of PRB. rRNA hybridization analysis indicated that F, C and SR were able to persist with PRB in continuous culture, and the addition of F, C and SR caused a large increase in ammonia concentration, particularly at high Trypticase concentrations. Monensin eliminated C and SR from the continuous cultures, and the steady state concentration of ammonia declined approximately 50%. Monensin was not able to eliminate F from the continuous cultures, and ammonia production was greater than PRB alone. The continuous culture studies provided a realistic model of monensin action in vivo. When cows were fed monensin, ruminal ammonia accumulation decreased, and the amount of rRNA that would hybridize with C and SR fell to undetectable concnetrations. F persisted in the rumen even if monensin was present, and its monensin resistance caused a 10% loss of feed protein.