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Objectives: High rates of carbapenem resistance in the human pathogen Acinetobacter baumannii threaten public health and need to be scrutinized.Methods: A total of 356 A. baumannii and 50 non-baumannii Acinetobacter spp. (NBA) strains collected in 2013 throughout South Korea were studied. The type of blaOXA-23 transposon was determined by PCR mapping and molecular epidemiology was assessed by MLST. Twelve representative strains and two comparative A. baumannii were entirely sequenced by single-molecule real-time sequencing.Results: The carbapenem resistance rate was 88% in A. baumannii, mainly due to blaOXA-23, with five exceptional cases associated with ISAba1-blaOXA-51-like. The blaOXA-23 gene in A. baumannii was carried either by Tn2006 (44%) or Tn2009 (54%), with a few exceptions carried by Tn2008 (1.6%). Of the NBA strains, 14% were resistant to carbapenems, two with blaOXA-58 and five with blaOXA-23 associated with Tn2006. The Tn2006-possessing strains belonged to various STs, whereas Tn2008- and Tn2009-possessing strains were limited to ST208 and ST191, respectively. The three transposons were often multiplied in the chromosome, and the gene copy number and the carbapenem MICs presented linear relationships either very strongly for Tn2008 or moderately for Tn2006 and Tn2009.Conclusions: The dissemination of Tn2006 was facilitated by its capability for intercellular transfer and that of Tn2009 was attributable to successful dissemination of the ST191 bacterial host carrying the transposon. Tn2008 was infrequent because of its insufficient ability to undergo intercellular transfer and the scarce bacterial host A. baumannii ST208. Gene amplification is an adaptive mechanism for bacteria that encounter antimicrobial drugs. [ABSTRACT FROM AUTHOR]

Objectives: The aac(6')-Ih gene encoding aminoglycoside 6'-N-acetyltransferase type I subtype h [AAC(6')-Ih] is plasmid-borne in Acinetobacter baumannii where it confers high-level amikacin resistance, but its origin remains unknown. We searched for the gene in the genomes of a collection of 133 Acinetobacter spp. and studied its species specificity, expression and dissemination.Methods: Gene copy number was determined by quantitative PCR, expression by quantitative RT-PCR, MIC by microdilution and transfer by plasmid mobilization.Results: The aac(6')-Ih gene was present in the chromosome of the two Acinetobacter gyllenbergii of the collection and was detected in all seven A. gyllenbergii clinical isolates. They had indistinguishable flanking regions indicating that the gene was intrinsic to this species. A. baumannii PIS Aba23 promoters were provided by insertion of ISAba23, which disrupted the Pnative promoter in A. gyllenbergii. Both types of promoters were similarly potent in Escherichia coli and A. baumannii. Aminoglycoside MICs for A. baumannii harbouring pIP1858 were higher than for A. gyllenbergii due to gene dosage. The non-self-transferable plasmid could be mobilized to other A. baumannii cells by the broad host range plasmid RP4.Conclusions: We have found the origin of aac(6')-Ih in A. gyllenbergii, a species isolated, although rarely, in humans, and documented that dissemination of this gene is restricted to the Acinetobacter genus. [ABSTRACT FROM AUTHOR]

Objectives: The in vitro pharmacodynamics of silver(I) and silver(II) complexes of a polydiguanide ligand, chlorhexidine, were assayed to examine the value of the bactericidal endpoint as an alternative means of evaluating their antibacterial activities against burn wound pathogens. [ABSTRACT FROM PUBLISHER]

: Objectives We identified Staphylococcus aureus strains having blunt inhibitory zones around the clindamycin or josamycin discs proximal to the erythromycin disc filled with slight bacterial growth. This ambiguous phenotype was termed as ‘macrolide–lincosamide–streptogramin B antimicrobial (MLSB) resistance having a foggy D-shaped inhibitory zone’ (fMLSB), and we tried to analyse its molecular mechanisms. : Methods Forty-one clinically isolated strains of fMLSB S. aureus were studied. The regulatory region of the erm(A) gene, which was found to be the only molecular mechanism of fMLSB, was sequenced. Then, β-galactosidase assays were performed to observe their expression patterns through the nucleotide sequential alteration. : Results According to the sequencing electropherogram, a grouping was made of a homogeneous nucleotide sequence group (73.2%) and a heterogeneous nucleotide sequence group (26.8%). The former group was composed of a 25 bp tandem duplication type and a 25 bp tandem triplication type. Their β-galactosidase activity was similar to that of constitutive MLSB resistance due to its high basal level. Nevertheless, the predicted mRNA secondary structure of the regulatory region maintains the stem–loops of inducible wild-type erm(A), and thereby its inducible character might be expected in vivo. Strains in the latter group were proven to have two different erm(A) genes, and then dual effect of expression was observed. : Conclusions The ambiguous phenotype of fMLSB is due to its possessing the dual character of inducible and constitutive expression of erm(A). The dual character is due to having one erm(A) gene of dual character or coexistence of two characterized erm(A) genes simultaneously. [ABSTRACT FROM AUTHOR]