scholarly journals Glycerol Monolaurate Inhibits Induction of Vancomycin Resistance in Enterococcus faecalis

1998 ◽  
Vol 180 (1) ◽  
pp. 182-185 ◽  
Author(s):  
Alexey Ruzin ◽  
Richard P. Novick
Keyword(s):  
Signal Transduction ◽  
Staphylococcus Aureus ◽  
Enterococcus Faecalis ◽  
Virulence Factor ◽  
Vancomycin Resistance ◽  
Exponential Phase ◽  
Glycerol Monolaurate ◽  
Initiation Of Transcription ◽  
Vancomycin Resistant ◽  
Virulence Factor Production

ABSTRACT Glycerol monolaurate (GML) is a surfactant that has been found to inhibit the post-exponential phase activation of virulence factor production and the induction of β-lactamase in Staphylococcus aureus. It has been suggested that signal transduction is the most probable target for GML (S. J. Projan, S. Brown-Skrobot, P. M. Schlievert, F. Vandenesch, and R. P. Novick, J. Bacteriol. 176:4204–4209, 1994). We found that GML suppresses growth of vancomycin-resistant Enterococcus faecalis on plates with vancomycin and blocks the induction of vancomycin resistance, which involves a membrane-associated signal transduction mechanism, either at or before initiation of transcription. Given the surfactant nature of GML and the results of previous experiments, we suggest that GML blocks signal transduction. In contrast, GML has no effect on the induction of erythromycin-inducible macrolide resistance in S. aureus, which does not involve signal transduction.

scholarly journals Equivalence of Lauric Acid and Glycerol Monolaurate as Inhibitors of Signal Transduction in Staphylococcus aureus

2000 ◽  
Vol 182 (9) ◽  
pp. 2668-2671 ◽  
Author(s):  
Alexey Ruzin ◽  
Richard P. Novick
Keyword(s):  
Signal Transduction ◽  
Staphylococcus Aureus ◽  
Enterococcus Faecalis ◽  
Mutant Strain ◽  
Virulence Factors ◽  
Lauric Acid ◽  
Inhibitory Activity ◽  
Null Mutant ◽  
Glycerol Monolaurate ◽  
Membrane Bound

ABSTRACT Glycerol monolaurate (GML) inhibits the expression of virulence factors in Staphylococus aureus and the induction of vancomycin resistance in Enterococcus faecalis, presumably by blocking signal transduction. Although GML is rapidly hydrolyzed by bacteria, one of the products, lauric acid, has identical inhibitory activity and is metabolized much more slowly. At least four distinct GML-hydrolyzing activities are identified in S. aureus: the secreted Geh lipase, residual supernatant activity in ageh-null mutant strain, a novel membrane-bound esterase, and a cytoplasmic activity.

scholarly journals Staphylococcus aureus Strains That are Hypersusceptible to Resistance Gene Transfer from Enterococci

2007 ◽  
Vol 51 (6) ◽  
pp. 2189-2191 ◽  
Author(s):  
Julia M.-L. Sung ◽  
Jodi A. Lindsay
Keyword(s):  
Staphylococcus Aureus ◽  
Gene Transfer ◽  
Resistance Gene ◽  
Enterococcus Faecalis ◽  
Vancomycin Resistance ◽  
Naturally Occurring ◽  
Resistance Transfer ◽  
Vancomycin Resistant ◽  
Restriction Modification

ABSTRACT We identified naturally occurring Staphylococcus aureus mutants of the restriction modification pathway SauI, including bovine lineage ST151. In a model of vancomycin resistance transfer from Enterococcus faecalis, ST151 isolates are 500 times more susceptible than human S. aureus isolates. The eradication of “hyperrecipient” strains may reduce the evolution of vancomycin-resistant S. aureus.

scholarly journals Total Synthesis of Xanthoangelol B and Its Various Fragments: Toward Inhibition of Virulence Factor Production of Staphylococcus aureus

2018 ◽  
Vol 61 (23) ◽  
pp. 10473-10487 ◽  
Author(s):  
Pushpak Mizar ◽  
Rekha Arya ◽  
Truc Kim ◽  
Soyoung Cha ◽  
Kyoung-Seok Ryu ◽  
...  
Keyword(s):  
Staphylococcus Aureus ◽  
Total Synthesis ◽  
Virulence Factor ◽  
Factor Production ◽  
Virulence Factor Production

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.

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