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Objectives: To determine the level of variation in the smeDEF efflux pump and smeT transcriptional regulator genes among three defined 16S rRNA sequence subgroups of clinical Stenotrophomonas maltophilia isolates.
Methods: smeDEF sequencing used a PCR genome walking approach. Determination of the sequence surrounding smeDEF used a flanking primer PCR method and specific primers anchored in smeD or smeF together with random primers.
Results: smeDEF is chromosomal and located in the same position in the chromosome in all three subgroups of isolates. Flanking smeD is a gene, smeT, encoding a putative transcriptional repressor for smeDEF. Variation at these loci among the isolates is considerably lower (up to 10%) than at intrinsic beta-lactamase loci (up to 30%) in the same isolates, implying greater functional constraint. The smeD-smeT intergenic region contains a highly conserved section, which maps with previously predicted promoter/operator regions, and a hypervariable untranslated region, which can be used to subgroup clinical isolates.
Conclusions: These data provide further evidence that it is possible to group clinical isolates of the inherently variable species, S. maltophilia, based on genotypic properties. Isolate D457, in which most work concerning smeDEF expression has been performed, does not fall into S. maltophilia subgroup A, which is the most typical.
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http://dx.doi.org/10.1093/jac/dkh367 | DOI Listing |
Front Cell Infect Microbiol
September 2025
Department of Respiratory Diseases, The Eighth Medical Center, Chinese People's Liberation Army General Hospital, Beijing, China.
Objective: To identify genes related to eravacycline resistance in () and to provide a theoretical basis for the study of eravacycline resistance mechanisms in and the development of new antibiotics.
Methods: The study employed an integrated omics approach: (1) antimicrobial susceptibility profiling via broth microdilution to determine baseline MICs for eravacycline and comparator drugs; (2) Induction of resistance in clinical isolates (WJ_4, WJ_14, WJ_18) with low eravacycline MICs through serial passage in escalating drug concentrations; (3) Transcriptome sequencing (RNA-seq) and whole-genome sequencing (WGS) of -induced resistant strains (WJ_4a, WJ_14a, WJ_18a) and a clinical high-MIC isolate (WJ_97); (4) Bioinformatics analyses, including differential gene expression screening (with |log2(fold change)| > 2 and FDR-adjusted p < 0.05), SNP detection via GATK, and copy number variation (CNV) quantification using CCNE-acc to identify and compare resistance-related genetic alterations.
J Antimicrob Chemother
August 2004
Bristol Centre for Antimicrobial Research and Evaluation, Department of Pathology & Microbiology, University of Bristol, School of Medical Sciences, University Walk, Bristol, BS8 1TD, UK.
Objectives: To determine the level of variation in the smeDEF efflux pump and smeT transcriptional regulator genes among three defined 16S rRNA sequence subgroups of clinical Stenotrophomonas maltophilia isolates.
Methods: smeDEF sequencing used a PCR genome walking approach. Determination of the sequence surrounding smeDEF used a flanking primer PCR method and specific primers anchored in smeD or smeF together with random primers.