Prevalence and Molecular Analysis of Macrolide and Fluoroquinolone Resistance among Isolates of
            <i>Streptococcus pneumoniae</i>
            Collected during the 2000-2001 PROTEKT US Study

Brown, Steven D.; Farrell, David J.; Morrissey, Ian

doi:10.1128/jcm.42.11.4980-4987.2004

Cited by 33 publications

(22 citation statements)

References 35 publications

(39 reference statements)

Supporting

Mentioning

Contrasting

Order By: Relevance

“…We presume that the high-level levofloxacin resistance of isolates with parE-only mutations was associated with efflux pump mechanisms (see below). The numerous QRDR mutations may not have any major effect on the fluoroquinolone MICs, as noted in a previous report (3). It is considered that for S. pneumoniae, ciprofloxacin is the drug most susceptible to efflux mechanisms (2,7,13,21).…”

Section: Distribution Of Macrolide Resistance Genes and Qrdr Mutationmentioning

confidence: 76%

Prevalence, Characteristics, and Molecular Epidemiology of Macrolide and Fluoroquinolone Resistance in Clinical Isolates of Streptococcus pneumoniae at Five Tertiary-Care Hospitals in Korea

Shin

Jung

Kim³

et al. 2007

Antimicrob Agents Chemother

View full text Add to dashboard Cite

The genes erm(B), mef(A), and both erm(B) and mef(A) were identified in 42.6, 10.1, and 47.3%, respectively, of the erythromycin-resistant Streptococcus pneumoniae isolates. Of the strains, 3.8% were nonsusceptible to levofloxacin and had 1 to 6 amino acid changes in the quinolone resistance-determining region, including a new mutation, Asn94Ser, in the product of parC. Levofloxacin with reserpine was highly specific for efflux screening.

show abstract

Section: Distribution Of Macrolide Resistance Genes and Qrdr Mutationmentioning

confidence: 76%

Prevalence, Characteristics, and Molecular Epidemiology of Macrolide and Fluoroquinolone Resistance in Clinical Isolates of Streptococcus pneumoniae at Five Tertiary-Care Hospitals in Korea

Shin

Jung

Kim³

et al. 2007

Antimicrob Agents Chemother

View full text Add to dashboard Cite

show abstract

“…The current prevention strategies based on immunogenic properties of capsular polysaccharides rely on a 23-valent and a 7-valent conjugate vaccine, even though the latter does not offer complete serotype coverage (3,10,26). Pneumococcal infection treatments are impaired by the increased number of clinical strains resistant to single or multiple antibiotherapies (11,39). There is a pressing need for the development of a vaccine with a wider serotype coverage spectrum as well as for the development of new drugs.…”

mentioning

confidence: 99%

Streptococcus pneumoniaeCholine-Binding Protein E Interaction with Plasminogen/Plasmin Stimulates Migration across the Extracellular Matrix

et al. 2008

View full text Add to dashboard Cite

The virulence mechanisms leading Streptococcus pneumoniae to convert from nasopharyngeal colonization to a tissue-invasive phenotype are still largely unknown. Proliferation of infection requires penetration of the extracellular matrix, which occurs by recruitment of host proteases to the bacterial cell surface. We present evidence supporting the role of choline-binding protein E (CBPE) (a member of the surface-exposed cholinebinding protein family) as an important receptor for human plasminogen, the precursor of plasmin. The results of ligand overlay blot analyses, solid-phase binding assays, and surface plasmon resonance experiments support the idea of an interaction between CBPE and plasminogen. We have shown that the phosphorylcholine esterase (Pce) domain of CBPE interacts with the plasminogen kringle domains. Analysis of the crystal structure of the Pce domain, followed by site-directed mutagenesis, allowed the identification of the plasminogen-binding region composed in part by lysine residues, some of which map in a linear fashion on the surface of the Pce domain. The biological relevance of the CBPE-plasminogen interaction is supported by the fact that, compared to the wild-type strain, a mutant of pneumococcus with the cbpE gene deleted (i) displays a reduced level of plasminogen binding and plasmin activation and (ii) shows reduced ability to cross the extracellular matrix in an in vitro model. These results support the idea of a physiological role for the CBPE-plasminogen interaction in pneumococcal dissemination into human tissue.

show abstract

“…Antibiotic treatment of these infections has become increasingly problematic due to an emergence of resistance to both penicillin and non-␤-lactam antibiotics. During the last decade, a rapid increase in the resistance of S. pneumoniae to macrolides has been observed in the United States (3,12,13,19,43).…”

mentioning

confidence: 99%

Macrolide Efflux in Streptococcus pneumoniae Is Mediated by a Dual Efflux Pump ( mel and mef ) and Is Erythromycin Inducible

Ambrose¹,

Nisbet²,

Stephens

2005

Antimicrob Agents Chemother

105

View full text Add to dashboard Cite

Macrolide resistance in Streptococcus pneumoniae due to efflux has emerged as an important worldwide clinical problem over the past decade. Efflux is mediated by the genes of the genetic element mega (macrolide efflux genetic assembly) and related elements, such as Tn1207.1. These elements contain two adjacent genes, mef (mefE or mefA) and the closely related mel gene ( . Previous studies have shown that Mef is required for macrolide resistance in S. pneumoniae; however, the contribution of Mel has not been fully determined. Independent deletions were constructed in mefE and mel in the serotype 14 macrolide-resistant strains GA16638 (erythromycin [Em] MIC, 8 to 16 g/ml) and GA17719 (Em MIC, 2 to 4 g/ml), which contain allelic variations in the mega element. The MICs to erythromycin were significantly reduced for the independent deletion mutants of both mefE and mel compared to those of the parent strains and further reduced threefold to fourfold to Em MICs of <0.15 g/ml with mefE mel double mutants. Using quantitative reverse transcription-PCR, the expression of mefE in the mel deletion mutants was increased more than 10-fold. However, in the mefE deletion mutants, the expression of mel did not differ significantly from the parent strains. The expression of both mefE and mel was inducible by erythromycin. These data indicate a requirement for both Mef and Mel in the novel efflux-mediated macrolide resistance system in S. pneumoniae and other gram-positive bacteria and that the system is inducible by macrolides.

show abstract

Prevalence and Molecular Analysis of Macrolide and Fluoroquinolone Resistance among Isolates of Streptococcus pneumoniae Collected during the 2000-2001 PROTEKT US Study

Cited by 33 publications

References 35 publications

Prevalence, Characteristics, and Molecular Epidemiology of Macrolide and Fluoroquinolone Resistance in Clinical Isolates of Streptococcus pneumoniae at Five Tertiary-Care Hospitals in Korea

Prevalence, Characteristics, and Molecular Epidemiology of Macrolide and Fluoroquinolone Resistance in Clinical Isolates of Streptococcus pneumoniae at Five Tertiary-Care Hospitals in Korea

Streptococcus pneumoniaeCholine-Binding Protein E Interaction with Plasminogen/Plasmin Stimulates Migration across the Extracellular Matrix

Macrolide Efflux in Streptococcus pneumoniae Is Mediated by a Dual Efflux Pump ( mel and mef ) and Is Erythromycin Inducible

Contact Info

Product

Resources

About