scholarly journals The Role of the Staphylococcal VraTSR Regulatory System on Vancomycin Resistance and vanA Operon Expression in Vancomycin-Resistant Staphylococcus aureus

PLoS ONE ◽  
2014 ◽  
Vol 9 (1) ◽  
pp. e85873 ◽  
Author(s):  
Nadia K. Qureshi ◽  
Shaohui Yin ◽  
Susan Boyle-Vavra
Keyword(s):  
Staphylococcus Aureus ◽  
Regulatory System ◽  
Vancomycin Resistance ◽  
Vancomycin Resistant ◽  
Operon Expression

Vancomycin Resistance Among Clinical Isolates of Staphylococcus aureus Obtained from Selected Hospitals in Sokoto Metropolis

2020 ◽  
pp. 111-116
Author(s):  
Umar A.I. ◽  
Keyword(s):  
Staphylococcus Aureus ◽  
Public Awareness ◽  
Vancomycin Resistance ◽  
Clinical Isolates ◽  
Resistant Bacteria ◽  
Major Public Health Problem ◽  
Drug Resistant ◽  
Sensitivity Testing ◽  
Vancomycin Resistant ◽  
Mic Value

The decreased vancomycin susceptibility and subsequent emergence of vancomycin resistant Staphylococcus aureus (VRSA) strains is a major public health problem. This study was aimed at detecting the prevalence of vancomycin resistant Staphylococcus aureus among clinical isolates obtained from patients attending Specialist Hospital Sokoto and Maryam Abacha Women and Children Hospital Sokoto. A total of 80 S. aureus clinical isolates were obtained from the medical microbiology laboratories of the selected hospitals. Antibiotic sensitivity testing of the isolates was carried out using the agar dilution method and isolates were screened for vancomycin resistance using vancomycin agar screen method. Of the 80 S. aureus isolates studied, 69 (86.0%) were identified as vancomycin susceptible S. aureus (VSSA) with MIC value of ≤2 µg/ml, 11 (13.8%) were identified as vancomycin intermediate S. aureus (VISA) and had MIC value of 4-8 µg/mL (VISA) and none of the isolates was identified as vancomycin resistant S. aureus (VRSA). The study detects high prevalence rate of VISA in the study area and identifies the need for increased public awareness on the danger associated with the presence of drug resistant bacteria. Emphasis should be directed at discouraging practices such as the use of over the counter medications which increase the rate of development of drug resistant organisms. Keywords: Vancomycin, Resistance, Staphylococcus aureus, MIC, VRSA

scholarly journals Penicillin-Binding Protein 2 Is Essential for Expression of High-Level Vancomycin Resistance and Cell Wall Synthesis in Vancomycin- Resistant Staphylococcus aureus Carrying the Enterococcal vanA Gene Complex

2004 ◽  
Vol 48 (12) ◽  
pp. 4566-4573 ◽  
Author(s):  
Anatoly Severin ◽  
Shang Wei Wu ◽  
Keiko Tabei ◽  
Alexander Tomasz
Keyword(s):  
Staphylococcus Aureus ◽  
Cell Wall ◽  
Binding Protein ◽  
Inducible Promoter ◽  
Protein Product ◽  
Vancomycin Resistance ◽  
Penicillin Binding Protein ◽  
Oxacillin Resistance ◽  
Vancomycin Resistant ◽  
High Level

ABSTRACT A combination of biochemical and genetic experiments were performed in order to better understand the mechanism of expression of high-level vancomycin resistance in Staphylococcus aureus. The transcription of pbp2 of the highly vancomycin- and oxacillin-resistant strain COLVA200 and its mutant derivative with inactivated mecA were put under the control of an inducible promoter, and the dependence of oxacillin and vancomycin resistance and cell wall composition on the concentration of the isopropyl-β-d-thiogalactopyranoside inducer was determined. The results indicate that mecA—the genetic determinant of oxacillin resistance—while essential for oxacillin resistance, is not involved with the expression of vancomycin resistance. Penicillin binding protein 2A, the protein product of mecA, appears to be unable to utilize the depsipeptide cell wall precursor produced in the vancomycin-resistant cells for transpeptidation. The key penicillin binding protein essential for vancomycin resistance and for the synthesis of the abnormally structured cell walls characteristic of vancomycin-resistant S. aureus (A. Severin, K. Tabei, F. Tenover, M. Chung, N. Clarke, and A. Tomasz, J. Biol. Chem. 279:3398-3407, 2004) is penicillin binding protein 2.

scholarly journals Genomic Analysis of the Emergence of Vancomycin-Resistant Staphylococcus aureus

mBio ◽  
2012 ◽  
Vol 3 (4) ◽  
Author(s):  
Scott D. Kobayashi ◽  
James M. Musser ◽  
Frank R. DeLeo
Keyword(s):  
United States ◽  
Staphylococcus Aureus ◽  
Dna Sequences ◽  
Clonal Complex ◽  
Infectious Agent ◽  
The United States ◽  
Vancomycin Resistance ◽  
Genetic Characteristics ◽  
Content Type ◽  
Vancomycin Resistant

ABSTRACT Staphylococcus aureus is a human commensal bacterium and a prominent cause of infections globally. The high incidence of S. aureus infections is compounded by the ability of the microbe to readily acquire resistance to antibiotics. In the United States, methicillin-resistant S. aureus (MRSA) is a leading cause of morbidity and mortality by a single infectious agent. Therapeutic options for severe MRSA infections are limited to a few antibiotics to which the organism is typically susceptible, including vancomycin. Acquisition of high-level vancomycin resistance by MRSA is a major concern, but to date, there have been only 12 vancomycin-resistant S. aureus (VRSA) isolates reported in the United States and all belong to a phylogenetic lineage known as clonal complex 5. To gain enhanced understanding of the genetic characteristics conducive to the acquisition of vancomycin resistance by S. aureus , V. N. Kos et al. performed whole-genome sequencing of all 12 VRSA isolates and compared the DNA sequences to the genomes of other S. aureus strains. The findings provide new information about the evolutionary history of VRSA and identify genetic features that may bear on the relationship between S. aureus clonal complex 5 strains and the acquisition of vancomycin resistance genes from enterococci.

scholarly journals STUDY OF VANCOMYCIN RESISTANCE AMONG STAPHYLOCOCCUS AUREUS

2019 ◽  
Vol 3 (6) ◽  
pp. 31-37
Author(s):  
Victor Victor Campos de Albuquerque ◽  
Vicente Clinton Justiniano Flores ◽  
Rubens Moura Campos Zeron ◽  
Bruno Bastos Godoi ◽  
Walberto Monteiro Neiva Eulálio Filho ◽  
...  
Keyword(s):  
Staphylococcus Aureus ◽  
Antibiotic Therapy ◽  
Bacterial Resistance ◽  
Vancomycin Resistance ◽  
Antimicrobial Drugs ◽  
Microbial Drug Resistance ◽  
Mechanism Of Resistance ◽  
Vana Gene ◽  
First Case ◽  
Vancomycin Resistant

Staphylococcus aureus (S.aureus) infections with Vancomycin resistance in hospital complexes are a concern, a significant increase in the number of these occurrences is observed since it is one of the last available antibiotic therapy routes available for the treatment of infectious processes bacterium. Thus, this work aims to present the main mechanism of resistance induction of S. aureus to Vancomycin. The research used the databases Medline, Scielo, the electronic site of the Google Scholar databases as well as specialized magazines in the area. Thus, the selected articles showed that in the late 1950s almost half of S. aureus strains were resistant to penicillin, and in the 1970s the first cases of methicillin-resistant S. aureus (MRSA) appeared; and thus, Vancomycin became employed in such cases. In 1996, the first case of S. aureus with intermediate resistance to vancomycin (VISA) was found. In 2002, the first case of Vancomycin-resistant S. aureus (VRSA) occurred, the latter being the only known to have the VanA gene until then. It was soon discovered that the emergence of this resistance occurred from the transfer of a plasmid with the transposon of the vancomycin resistant vanA, Tn1546 vancomycin (VRE) gene to an MRSA, which already had a plasmid for resistance to gentamicin and production of beta-lactamase. This new plasmid was disseminated to other S. aureus and thus disseminating a new resistance. Thus, the conclusion is that the cycle repeats itself and previously sensitive bacteria become resistant; thus, in this rhythm of emergence of bacterial resistance against antibiotic therapy is worrying, there will be a moment when there will be no antibiotic capable of acting in the fight against bacteria. This shows the need to understand the mechanism of resistance, the discovery of new antimicrobial drugs and the prevention of the spread of resistant microbes.Key words: Staphylococcus aureus, vancomycin, microbial drug resistance, vancomycin resistance.

scholarly journals Mutated Response Regulator graR Is Responsible for Phenotypic Conversion of Staphylococcus aureus from Heterogeneous Vancomycin-Intermediate Resistance to Vancomycin-Intermediate Resistance

2007 ◽  
Vol 52 (1) ◽  
pp. 45-53 ◽  
Author(s):  
Hui-min Neoh ◽  
Longzhu Cui ◽  
Harumi Yuzawa ◽  
Fumihiko Takeuchi ◽  
Miki Matsuo ◽  
...  
Keyword(s):  
Staphylococcus Aureus ◽  
Whole Genome Sequencing ◽  
Genome Sequencing ◽  
Response Regulator ◽  
Regulatory System ◽  
Vancomycin Resistance ◽  
Whole Genome ◽  
Two Component ◽  
Intermediate Resistance ◽  
Mrsa Strains

ABSTRACT Multistep genetic alteration is required for methicillin-resistant Staphylococcus aureus (MRSA) to achieve the level of vancomycin resistance of vancomycin-intermediate S. aureus (VISA). In the progression of vancomycin resistance, strains with heterogeneous vancomycin resistance, designated hetero-VISA, are observed. In studying the whole-genome sequencing of the representative hetero-VISA strain Mu3 and comparing it with that of closely related MRSA strains Mu50 (VISA) and N315 (vancomycin-susceptible S. aureus [VSSA]), we identified a mutation in the response regulator of the graSR two-component regulatory system. Introduction of mutated graR, designated graR*, but not intact graR, designated graRn, could convert the hetero-VISA phenotype of Mu3 into a VISA phenotype which was comparable to that of Mu50. The same procedure did not appreciably increase the vancomycin resistance of VSSA strain N315, indicating that graR* expression was effective only in the physiological milieu of hetero-VISA cell to achieve a VISA phenotype. Interestingly, the overexpression of graR* increased the daptomycin MICs in both Mu3 and N315 and decreased the oxacillin MIC in N315.

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