Background: Vancomycin (glycopeptide)-resistant enterococci (VRE or GRE) can cause serious problems for hospitalized patients due to the limited options for treatment of VRE infections. As infection with VRE increases in hospitals, further knowledge about vancomycin resistant genes is needed.
Methods: Isolates of Enterococcus spp. were collected from hospitalized patients in Tehran (Iran) during 2006. Detailed molecular analysis was performed for vancomycin resistance genotype and vanHAX using conventional PCR and PCR- RFLP (restriction fragment length polymorphism), respectively.
Results: out of 830 enterococci spp., 48 VRE isolates (5.8 percent) were obtained. All of VRE isolates carried vanA gene. DdeI digestion of vanHAX element showed the presence of point mutation at 8234 position.
Conclusion: This study indicates that vanA is a predominant genotype in Iranian isolates. In addition, PCR-RFLP analysis revealed the presence of two types of vanHAX element in vanA harboring transposons.
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Genes (Basel)
October 2022
Department of Biotechnology and Life Sciences, University of Insubria, 21100 Varese, Italy.
Clinically relevant glycopeptide antibiotics remain among the most successful classes of natural antibacterials. This success, however, is endangered by the spread of glycopeptide resistance genes, also known as genes. Thus, it is important to trace and comprehend possible routes of gene dissemination.
View Article and Find Full Text PDFInt J Antimicrob Agents
April 2022
Department of Microbiology and Virology, Faculty of Natural Sciences, Comenius University in Bratislava, Slovakia. Electronic address:
Objectives: Hospital vancomycin-resistant Enterococcus faecium (VREfm) were evaluated in term of resistance and phylogenetic relatedness to estimate the location and possible route of transmission of resistance determinants.
Methods: Hospital VREfm (n = 49) were collected in the northern part of Slovakia during 2017-2020. The collection was analysed for the presence of the van operon and 10 representatives were subjected to whole-genome sequencing using Illumina MiSeq platform.
Antimicrob Agents Chemother
July 2016
Research Group for Host-Microbe Interactions, Department of Medical Biology, Faculty of Health Sciences, University of Tromsø-The Arctic University of Norway, Tromsø, Norway Norwegian National Advisory Unit on Detection of Antimicrobial Resistance, Department of Microbiology and Infection Control, University Hospital of North-Norway, Tromsø, Norway
We report an outbreak of vancomycin-variable vanA(+) enterococci (VVE) able to escape phenotypic detection by current guidelines and demonstrate the molecular mechanisms for in vivo switching into vancomycin resistance and horizontal spread of the vanA cluster. Forty-eight vanA(+) Enterococcus faecium isolates and one Enterococcus faecalis isolate were analyzed for clonality with pulsed-field gel electrophoresis (PFGE), and their vanA gene cluster compositions were assessed by PCR and whole-genome sequencing of six isolates. The susceptible VVE strains were cultivated in brain heart infusion broth containing vancomycin at 8 μg/ml for in vitro development of resistant VVE.
View Article and Find Full Text PDFIran Biomed J
October 2008
Dept. of Bacteriology, School of Public Health, Tehran University/Medical Sciences, Tehran, Iran.
Background: Vancomycin (glycopeptide)-resistant enterococci (VRE or GRE) can cause serious problems for hospitalized patients due to the limited options for treatment of VRE infections. As infection with VRE increases in hospitals, further knowledge about vancomycin resistant genes is needed.
Methods: Isolates of Enterococcus spp.
J Med Microbiol
January 2008
Microbiology Laboratory, Department of Physiology, University College of Science, Technology and Agriculture, University of Calcutta, Kolkata, India.
A pathogenic vancomycin-resistant Staphylococcus aureus (VRSA) isolate (MIC > or =64 microg ml(-1)) was obtained from a Kolkata hospital in June 2005. Species identification was confirmed by Gram staining, standard biochemical tests and PCR amplification of the nuc gene, which encodes the thermostable nuclease that is highly specific for S. aureus.
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