In Vitro Activity of Novel Rifamycins against Rifamycin-Resistant
            <i>Staphylococcus aureus</i>

Murphy, Christian; Mullin, Steve; Osburne, Marcia S.; Duzer, John van; Siedlecki, Jim; Yu, Xiang; Kerstein, Kathy; Cynamon, Michael H.; Rothstein, David M.

doi:10.1128/aac.50.3.827-834.2006

Cited by 36 publications

(45 citation statements)

References 45 publications

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“…From this extensive global repository, we provide novel and valuable information about the genetic diversity of CNS species that cause endocarditis, suggesting b Regions known to be involved with resistance to rifampin (15).…”

Section: Discussionmentioning

confidence: 99%

“…Nucleotide and amino acid sequence alignments and phylogenetic trees were constructed by the neighbor-joining method with Kimura's two-parameter distance correction model and 1,000 bootstrap replications in the MEGA version 3.1 software package (11). Rifampin resistance was evaluated by using the rifampin resistance-determining region of the rpoB gene as described by Murphy et al (15) for all strains of CNS.…”

Section: Methodsmentioning

confidence: 99%

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Genotypic Diversity of Coagulase-Negative Staphylococci Causing Endocarditis: a Global Perspective

et al. 2008

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Coagulase-negative staphylococci (CNS) are important causes of infective endocarditis (IE), but their microbiological profiles are poorly described. We performed DNA target sequencing and susceptibility testing for 91 patients with definite CNS IE who were identified from the International Collaboration on Endocarditis-Microbiology, a large, multicenter, multinational consortium. A hierarchy of gene sequences demonstrated great genetic diversity within CNS from patients with definite endocarditis that represented diverse geographic regions. In particular, rpoB sequence data demonstrated unique genetic signatures with the potential to serve as an important tool for global surveillance.Coagulase-negative staphylococci (CNS) are increasingly important causes of community-and health care-associated infective endocarditis (7,12,17). Although more than 40 species make up this heterogeneous group of microorganisms, identification of CNS to the species level often is not performed because of laboratory uncertainty about its clinical relevance or the absence of reliable identification systems (10). There is, however, growing evidence that identification of CNS to the species level may alter diagnostic and therapeutic clinical decision making where specific species have unique virulence factors (e.g., Staphylococcus lugdunensis) (2) or unusual antibacterial resistance patterns (e.g., glycopeptide resistance with S. epidermidis and S. haemolyticus) (4-6). In recent years, partial 16S rRNA gene sequencing has emerged as an accurate and reliable method to identify CNS, but this molecular target is limited by having less than 1% sequence divergence among some CNS species. Alternative gene targets such as tuf (elongation factor Tu) (10) and rpoB (RNA polymerase ␤ subunit) (9, 14) have been evaluated, but to our knowledge, no studies have applied gene sequencing of these targets from patients with definite CNS endocarditis.Given the limited frequency of CNS endocarditis in a single institution, the International Collaboration on EndocarditisMicrobiology (ICE-Micro), a large, multicenter, multinational consortium, provided a unique opportunity to improve our understanding of the spectrum of CNS microorganisms implicated in prosthetic and native valve endocarditis. We performed gene sequencing with multiple DNA targets to identify CNS from patients with definite endocarditis to the species level. We also evaluated the potential for a hierarchy of sequence data to provide greater specificity for species identification, serve as an epidemiologic tool to assess clonality, and predict antimicrobial resistance. MATERIALS AND METHODSCNS isolates from patients with definite endocarditis were submitted by ICEMicro investigators representing a collection from 18 medical centers in 12 countries. Conventional identification and susceptibility testing were performed at a central laboratory with a commercially available panel processed on the Microscan Walkaway instrument (PC-21; Dade Behring, Deerfield, IL) by a

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Section: Discussionmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

Genotypic Diversity of Coagulase-Negative Staphylococci Causing Endocarditis: a Global Perspective

et al. 2008

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“…Interestingly, the H502N mutation has been associated with intermediate resistance to rifamycins, but never to high-level resistance (6, 18), as we found, which may indicate a separate mechanism of resistance in C. difficile. These SLPs in the rpoB gene are conserved in many genera of rifamycin-resistant bacteria, as demonstrated by sequence alignments (6,16,18).…”

mentioning

confidence: 99%

“…Position S498 in the C. difficile rpoB gene corresponds to A477 in Staphylococcus aureus, which has been linked to rifamycin resistance. Both new SLPs occur in amino acids in Taq polymerase that do not interact directly with rifamycins in the binding pocket (3,16), suggesting that the most likely mechanism of action is structural modification of the binding pocket and lowered affinity of rpoB for rifamycins. The other two previously described mutations found in our study, H502N and R505K, are believed to affect the direct interaction of rpoB with the rifamycins.…”

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confidence: 99%

Divergent Rifamycin Susceptibilities of Clostridium difficile Strains in Canada and Italy and Predictive Accuracy of Rifampin Etest for Rifamycin Resistance

et al. 2011

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We tested the activities of rifampin (RIF) and rifaximin (RFX) against 180 Clostridium difficile clinical isolates selected from Canadian and Italian culture collections. MICs were determined by CLSI agar dilution for both drugs and by Etest for RIF. Sixteen of 85 Italian isolates (18.8%) showed high-level resistance to both rifamycins (MICs, >16 g/ml), compared to 2 of 95 (2.1%) Canadian isolates. Two new rpoB mutations were identified in rifamycin-resistant isolates. RIF susceptibility by Etest correlated completely with susceptibility to both rifamycins determined by agar dilution.

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“…The change in bacterial density in the lung tissues was calculated by subtracting the mean log 10 CFU of the control mice sacrificed just prior to dosing from the mean log 10 CFU of the drug treated and control mice at the end of 6 or 24 hours of therapy. Antibiotic-carry over was observed upon culturing the lung homogenates after the 3 doses of ABI-0043 80 mg/kg q8h, and as such, the limit of detection was 2ϫ10 4 CFU for this group. Fig.…”

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confidence: 75%

Bactericidal Efficacy of ABI-0043, a Novel Rifamycin, in a Murine Pneumococcal Pneumonia Model

et al. 2006

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In Vitro Activity of Novel Rifamycins against Rifamycin-Resistant Staphylococcus aureus

Cited by 36 publications

References 45 publications

Genotypic Diversity of Coagulase-Negative Staphylococci Causing Endocarditis: a Global Perspective

Genotypic Diversity of Coagulase-Negative Staphylococci Causing Endocarditis: a Global Perspective

Divergent Rifamycin Susceptibilities of Clostridium difficile Strains in Canada and Italy and Predictive Accuracy of Rifampin Etest for Rifamycin Resistance

Bactericidal Efficacy of ABI-0043, a Novel Rifamycin, in a Murine Pneumococcal Pneumonia Model

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