scholarly journals Epidemiology and Clinical Impact of Glycopeptide Resistance in Staphylococcus aureus

Infection ◽  
2004 ◽  
Vol 32 (6) ◽  
pp. 315-327 ◽  
Author(s):  
C. Ruef
PLoS ONE ◽  
2011 ◽  
Vol 6 (6) ◽  
pp. e21577 ◽  
Author(s):  
Adriana Renzoni ◽  
Diego O. Andrey ◽  
Ambre Jousselin ◽  
Christine Barras ◽  
Antoinette Monod ◽  
...  

2012 ◽  
Vol 4 (1) ◽  
pp. 20 ◽  
Author(s):  
Siti Roszilawati Ramli ◽  
Hui-min Neoh ◽  
Muhammad Nazri Aziz ◽  
Salasawati Hussin

In a 3-month study done in Hospital Kuala Lumpur (HKL), 7 out of 320 methicillin resistant <em>Staphylococcus aureus </em>isolates were confirmed as heterogeneous vancomycin intermediate S. aureus (hVISA) using the glycopeptide resistance detection e-test and population analysis, giving a prevalence rate of 2.19%. This is the first report of hVISA in Malaysia.


2015 ◽  
Vol 7 (3) ◽  
pp. 97 ◽  
Author(s):  
Divya Deodhar ◽  
George Varghese ◽  
Veeraraghavan Balaji ◽  
James John ◽  
Grace Rebekah ◽  
...  

2006 ◽  
Vol 50 (11) ◽  
pp. 3622-3630 ◽  
Author(s):  
Bruno Périchon ◽  
Patrice Courvalin

ABSTRACT Vancomycin resistance of Staphylococcus aureus NY-VRSA and VRSA-5 is due to acquisition of a vanA operon located in a Tn1546-like element. The vanA gene cluster of NY-VRSA contained one copy of insertion sequences IS1251 and IS1216V relative to that of VRSA-5. As evidenced by the nature of the late peptidoglycan precursors and by quantification of d,d-peptidase activities, the vancomycin resistance genes were efficiently expressed in both strains. Study of the stability and inducibility of glycopeptide resistance suggested that low-level glycopeptide resistance of NY-VRSA was most probably due to plasmid instability combined with a long delay for resistance induction. The activity of combinations of vancomycin or teicoplanin with oxacillin against the four VanA-type S. aureus strains already reported was tested by single and double disk diffusion, E-test on agar alone or supplemented with antibiotics, the checkerboard technique, and by determining time-kill curves. A strong synergism against the four clinical isolates, with fractional inhibitory concentration indexes from 0.008 to 0.024, was reproducibly observed between the two antibiotics by all methods. These observations indicate that cell wall inhibitors of the β-lactam and glycopeptide classes exert strong and mutual antagonistic effects on resistance to each other against VanA-type methicillin-resistant S. aureus.


2018 ◽  
Vol 5 (suppl_1) ◽  
pp. S70-S70
Author(s):  
Jessica Gulliver ◽  
Brittney Jung-Hynes ◽  
Derrick Chen

Abstract Background Methicillin-susceptible/methicillin-resistant Staphylococcus aureus (MSSA/MRSA) can be directly identified from positive blood culture bottles using molecular methods. This provides faster results than traditional phenotypic testing, but discrepancies between the two are occasionally found. We sought to determine the incidence and clinical impact of such discrepancies. Methods Positive blood culture bottles are routinely tested in the hospital clinical laboratory for mecA via Xpert MRSA/SA BC (PCR), and antimicrobial susceptibility testing (AST) via MicroScan PC33 is performed on recovered S. aureus isolates; discrepancies between PCR and AST are resolved by repeat and supplemental (Kirby-Bauer) testing. A retrospective review of medical and laboratory data from January 2015 to December 2017 was performed on all patients that had discordant PCR and AST results. Results Approximately 1,200 PCR assays were performed from January 2015 to December 2017, and there were 5 (0.4%) cases with discordant AST Results. Four cases were classified as MSSA by PCR but MRSA by AST, and 1 case was classified as MRSA by PCR but MSSA by AST. For the former group, antimicrobial therapy was changed in 2 patients to cover MRSA and 1 patient was readmitted, while the remaining 2 patients were already being treated for MRSA; for the latter case, this patient was treated for MRSA during the initial hospitalization, but was readmitted with disseminated MSSA and subsequently deceased. Based on genetic targets identified by PCR and cefoxitin and oxacillin AST, discrepancies were likely due to borderline oxacillin resistance (BORSA) (n = 1), presence of an SCCmec variant not detected by PCR (n = 1), or undetermined (n = 3). Conclusion Rapid identification of MRSA bacteremia via PCR provides actionable information to direct empiric treatment. While highly accurate, PCR results are infrequently not corroborated by AST. This rare possibility should be considered when modifying therapy based on initial PCR results, and there should be close communication between the clinical team and laboratory for these challenging cases. Disclosures All authors: No reported disclosures.


mSphere ◽  
2018 ◽  
Vol 3 (1) ◽  
Author(s):  
Romain Guérillot ◽  
Anders Gonçalves da Silva ◽  
Ian Monk ◽  
Stefano Giulieri ◽  
Takehiro Tomita ◽  
...  

Increasing antibiotic resistance in the major human pathogen Staphylococcus aureus is threatening the ability to treat patients with these infections. Recent laboratory studies suggest that mutations in the gene commonly associated with rifampin resistance may also impact susceptibility to other last-line antibiotics in S. aureus; however, the overall frequency and clinical impact of these mutations are unknown. By mining a global collection of clinical S. aureus genomes and by mutagenesis experiments, this work reveals that common rifampin-induced rpoB mutations promote phenotypic plasticity that has led to the global emergence of stable, multidrug-resistant S. aureus lineages that are associated with increased risk of therapeutic failure through coresistance to other last-line antimicrobials. We recommend decreasing susceptibility breakpoints for rifampin to allow phenotypic detection of critical rpoB mutations conferring low resistance to rifampin and reconsidering the appropriate use of rifampin to reduce the fixation and spread of these deleterious mutations globally.


2009 ◽  
Vol 58 (3) ◽  
pp. 376-380 ◽  
Author(s):  
Andrew Kirby ◽  
Kavya Mohandas ◽  
Caroline Broughton ◽  
Timothy J. Neal ◽  
Godfrey W. Smith ◽  
...  

We report a patient who developed a meticillin-resistant Staphylococcus aureus (MRSA) central venous catheter infection complicated by infective endocarditis. The patient was initially treated with glycopeptides, which led to the development of heterogeneous glycopeptide resistance, the detection of which required the use of a macro Etest screening test. Subsequently, the causative strain, confirmed by PFGE as a UK epidemic MRSA-15, was treated with daptomycin, and again resistance developed in vivo. The development in vivo of resistance to both these agents suggests that the resistance mechanisms may be associated. We suggest that the clinician managing MRSA infection should anticipate daptomycin resistance when reduced glycopeptide susceptibility is detected.


2004 ◽  
Vol 48 (8) ◽  
pp. 2958-2965 ◽  
Author(s):  
Adriana Renzoni ◽  
Patrice Francois ◽  
Dongmei Li ◽  
William L. Kelley ◽  
Daniel P. Lew ◽  
...  

ABSTRACT The impact of glycopeptide resistance on the molecular regulation of Staphylococcus aureus virulence and attachment to host tissues is poorly documented. We compared stable teicoplanin-resistant methicillin-resistant S. aureus (MRSA) strain 14-4 with its teicoplanin-susceptible MRSA parent, strain MRGR3, which exhibits a high degree of virulence in a rat model of chronic foreign body MRSA infection. The levels of fibronectin-mediated adhesion and surface display of fibronectin-binding proteins were higher in teicoplanin-resistant strain 14-4 than in its teicoplanin-susceptible parent or a teicoplanin-susceptible revertant (strain 14-4rev) that spontaneously emerged during tissue cage infection. Quantitative reverse transcription-PCR (qRT-PCR) showed four- and twofold higher steady-state levels of fnbA and fnbB transcripts, respectively, in strain 14-4 than in its teicoplanin-susceptible counterparts. Analysis of global regulatory activities by qRT-PCR revealed a strong reduction in the steady-state levels of RNAIII and RNAII in the teicoplanin-resistant strain compared to in its teicoplanin-susceptible counterparts. In contrast, sarA mRNA levels were more than fivefold higher in strain 14-4 than in MRGR3 and 14-4rev. Furthermore, the alternative transcription factor sigma B had a higher level of functional activity in the teicoplanin-resistant strain than in its teicoplanin-susceptible counterparts, as evidenced by significant increases in both the sigma B-dependent asp23 mRNA levels and the sarA P3 promoter-derived transcript levels, as assayed by qRT-PCR and Northern blotting, respectively. These data provide further evidence that the emergence of glycopeptide resistance is linked by still poorly understood molecular pathways with significant pleiotropic changes in the expression and regulation of some major virulence genes. These molecular and phenotypic changes may have a profound impact on the bacterial adhesion and colonization properties of such multiresistant organisms.


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