Isogenic L1 and L2 gene knockout mutants of Stenotrophomonas maltophilia KJ (KJ⌬L1 and KJ⌬L2, respectively) were constructed by xylE gene replacement. Induction kinetics of the L1 and L2 genes were evaluated by testing catechol 2,3-dioxygenase activity in the mutants. The results suggested that the induction of the L1 and L2 genes was differentially regulated.

BackgroundThe prevalence of resistance to fusidic acid of methicillin-resistant Staphylococcus aureus (MRSA) was increased each year in a Taiwan hospital. Thirty-four MRSA clinical isolates collected in 2007 and 2008 with reduced susceptibility to FA were selected for further evaluation the presence of resistance determinants.ResultsThe most common resistance determinant was fusC, found in 25 of the 34 MRSA isolates. One of the 25 fusidic acid-resistant MRSA harboured both fusB and fusC, which is the first time this has been identified. Mutations in fusA were found in 10 strains, a total of 3 amino-acid substitutions in EF-G (fusA gene) were detected. Two substitutions with G556S and R659L were identified for the first time. Low-level resistance to fusidic acid (MICs, ≤ 32 μg/ml) was found in most our collection. All collected isolates carried type III SCCmec elements. MLST showed the isolates were MRSA ST239. PFGE revealed nine different pulsotypes in one cluster.ConclusionsOur results indicate that the increase in the number of fusidic acid resistant among the MRSA isolates in this hospital is due mainly to the distribution of fusC determinants. Moreover, more than one fusidic acid-resistance mechanism was first detected in a same stain in our collection.

No abstract

Arylamine N-acetyltransferase (NAT) activities with p-aminobenzoic acid (PABA) and 2-aminofluorene (AF) were determined in H. pylori collected from peptic ulcer patients. Cytosols or suspensions of H. pylori with or without different concentrations of aloe-emodin co-treatment showed different percentages of AF and PABA acetylation. The data indicate that there was decreased NAT activity associated with increased aloe-emodin in H. pylori cytosols. Inhibition of growth study from H. pylori demonstrated that aloe-emodin elicited dose-dependent growth inhibition in H. pylori cultures. The report is the first finding of aloe-emodin inhibition of arylamine NAT activity in a strain of H. pylori.