ABSTRACT
The RapID-ANA System (Innovative Diagnostics Systems, Inc., Atlanta, Ga.) was used to test 102 strains of 14 species of phenotypically similar bile-inhibited Bacteroides from humans. Bacteroides oris, Bacteroides veroralis, Bacteroides buccalis, Bacteroides melaninogenicus, Bacteroides loescheii, and Bacteroides denticola had very similar enzyme activity profiles. Clear differentiation of these six species by the RapID-ANA System was not possible, but tests for arginine aminopeptidase and beta-glucosidase were helpful. Bacteroides oralis, Bacteroides intermedius, Bacteroides corporis, Bacteroides disiens, Bacteroides bivius, Bacteroides gingivalis, Bacteroides asaccharolyticus, and Bacteroides buccae each had unique enzyme activity profiles. No consistent differences in enzyme activities were found between the two DNA homology groups within Bacteroides melaninogenicus, Bacteroides loescheii, or Bacteroides intermedius. Tests for glycine aminopeptidase, alpha-galactosidase, arginine aminopeptidase, alpha-fucosidase, N-acetylglucosaminidase, reduction of triphenyltetrazolium, and production of indole were helpful in the differentiation of the species studied.
Subject(s)
Bacteroides/enzymology , Hydrolases/metabolism , Acetylglucosaminidase/metabolism , Aminopeptidases/metabolism , Bacteroides/classification , Bacteroides/growth & development , Bile/physiology , Humans , Prevotella melaninogenica/classification , Prevotella melaninogenica/enzymology , Prevotella melaninogenica/growth & development , Species Specificity , Tetrazolium Salts/metabolism , Tryptophanase/metabolism , alpha-Galactosidase/metabolism , alpha-L-Fucosidase/metabolismABSTRACT
Monensin inhibited methanogenesis from formate but not from H(2)-CO(2) by resting-cell suspensions of Methanobacterium formicicum. The antibiotic severely inhibited growth on formate. The lag phase of H(2)-CO(2)-grown cultures was prolonged by monensin, but these cultures recovered from the initial inhibition. The recovery did not result from the development of a monensin-resistant population or inactivation of the antibiotic.
