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

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          Abstract

          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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          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.

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              Reduced vancomycin susceptibility in Staphylococcus aureus, including vancomycin-intermediate and heterogeneous vancomycin-intermediate strains: resistance mechanisms, laboratory detection, and clinical implications.

              The emergence of vancomycin-intermediate Staphylococcus aureus (VISA) and heterogeneous vancomycin-intermediate Staphylococcus aureus (hVISA) over the past decade has provided a challenge to diagnostic microbiologists to detect these strains, clinicians treating patients with infections due to these strains, and researchers attempting to understand the resistance mechanisms. Recent data show that these strains have been detected globally and in many cases are associated with glycopeptide treatment failure; however, more rigorous clinical studies are required to clearly define the contribution of hVISA to glycopeptide treatment outcomes. It is now becoming clear that sequential point mutations in key global regulatory genes contribute to the hVISA and VISA phenotypes, which are associated predominately with cell wall thickening and restricted vancomycin access to its site of activity in the division septum; however, the phenotypic features of these strains can vary because the mutations leading to resistance can vary. Interestingly, changes in the staphylococcal surface and expression of agr are likely to impact host-pathogen interactions in hVISA and VISA infections. Given the subtleties of vancomycin susceptibility testing against S. aureus, it is imperative that diagnostic laboratories use well-standardized methods and have a framework for detecting reduced vancomycin susceptibility in S. aureus.
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                Author and article information

                Journal
                1886
                European Journal of Microbiology and Immunology
                EuJMI
                Akadémiai Kiadó
                2062-8633
                March 2018
                : 8
                : 1
                : 25-30
                Affiliations
                [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

                Article
                10.1556/1886.2018.00003
                5944423
                1ad84332-7b3a-4018-9295-ad2e1b854db4
                © 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.

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

                Medicine,Immunology,Health & Social care,Microbiology & Virology,Infectious disease & Microbiology
                VISA,VRSA,MRSA,phenotypic,molecular,E-test

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