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      Phenotypic and molecular identification of vancomycin resistance in clinical Staphylococcus aureus isolates in Osogbo, Nigeria


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          The use of vancomycin for treatment of serious infections caused by MRSA strains has resulted in emergence of vancomycin-resistant Staphylococcus aureus (VRSA) in clinical settings. Following our previous report of phenotypic VRSA in Nigeria, the current study attempts to determine the genetic basis underlying this resistance. Over a period of 6 months, non-duplicate clinical S. aureus isolates from 73 consecutive patients with infective conditions at Ladoke Akintola University of Technology Teaching Hospital, Osogbo were tested against a panel of eight selected antibiotics by disk diffusion test. The Epsilom test strip was used to determine vancomycin minimum inhibitory concentration (MIC) and polymerase chain reaction (PCR) assay to amplify nuc, mecA, vanA, and vanB genes. Of 73 isolates, 61 (83.6%) had MIC of ≤2 μg/ml, 11 (15.1%) had 4–8 μg/ml and 1 (1.4%) had 16 μg/ml. The mecA gene was detected in 5 (6.8%) isolates but none contained vanA or vanB genes. Both vancomycin-susceptible and intermediate isolates were resistant to multiple antibiotics, while the only vancomycin resistant isolate was resistant to all eight antibiotics. The result confirms the occurrence of phenotypic vancomycin intermediate-resistant S. aureus (VISA) and VRSA infections in Nigeria, but the molecular basis will require further investigation.

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          Methicillin-resistant Staphylococcus aureus clinical strain with reduced vancomycin susceptibility.

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            Genetic analysis of a high-level vancomycin-resistant isolate of Staphylococcus aureus.

            Vancomycin is usually reserved for treatment of serious infections, including those caused by multidrug-resistant Staphylococcus aureus. A clinical isolate of S. aureus with high-level resistance to vancomycin (minimal inhibitory concentration = 1024 microg/ml) was isolated in June 2002. This isolate harbored a 57.9-kilobase multiresistance conjugative plasmid within which Tn1546 (vanA) was integrated. Additional elements on the plasmid encoded resistance to trimethoprim (dfrA), beta-lactams (blaZ), aminoglycosides (aacA-aphD), and disinfectants (qacC). Genetic analyses suggest that the long-anticipated transfer of vancomycin resistance to a methicillin-resistant S. aureus occurred in vivo by interspecies transfer of Tn1546 from a co-isolate of Enterococcus faecalis.
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              Plasmid-mediated resistance to vancomycin and teicoplanin in Enterococcus faecium.


                Author and article information

                European Journal of Microbiology and Immunology
                Akadémiai Kiadó
                March 2018
                : 8
                : 1
                : 25-30
                [1]Department of Medical Microbiology and Parasitology, College of Health Sciences, Ladoke Akintola University of Technology , PMB 4400, Osogbo, Nigeria
                Author notes
                [ * ]

                Corresponding author: Taiwo Samuel Sunday; sstaiwo@ 123456lautech.edu.ng

                © 2018 The Author(s)

                This is an open-access article distributed under the terms of the Creative Commons Attribution-NonCommercial 4.0 International License (https://creativecommons.org/licenses/by-nc/4.0/), which permits unrestricted use, distribution, and reproduction in any medium for non-commercial purposes, provided the original author and source are credited, a link to the CC License is provided, and changes - if any - are indicated.

                : 27 January 2018
                : 18 February 2018
                Page count
                Pages: 6
                Original Research Paper

                Medicine,Immunology,Health & Social care,Microbiology & Virology,Infectious disease & Microbiology


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