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Pregled bibliografske jedinice broj: 1225240

Macrolide hyper-susceptibility is associated with the abscence of efflux mechanism in clinical isolates of H. influenzae


Bozdogan, Bulent; Peric, Mihaela; Jacobs, Michael R; Appelbaum, Peter C.
Macrolide hyper-susceptibility is associated with the abscence of efflux mechanism in clinical isolates of H. influenzae // 42nd ICAAC Abstracts, ASM
San Diego (CA), Sjedinjene Američke Države: ASM, 2002. str. 76-76 (poster, međunarodna recenzija, sažetak, znanstveni)


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Naslov
Macrolide hyper-susceptibility is associated with the abscence of efflux mechanism in clinical isolates of H. influenzae

Autori
Bozdogan, Bulent ; Peric, Mihaela ; Jacobs, Michael R ; Appelbaum, Peter C.

Vrsta, podvrsta i kategorija rada
Sažeci sa skupova, sažetak, znanstveni

Izvornik
42nd ICAAC Abstracts, ASM / - : ASM, 2002, 76-76

Skup
42nd ICAAC, ASM

Mjesto i datum
San Diego (CA), Sjedinjene Američke Države, 27.09.2002. - 30.09.2002

Vrsta sudjelovanja
Poster

Vrsta recenzije
Međunarodna recenzija

Ključne riječi
macrolide, susceptibility, H. Influenzae

Sažetak
Background. Macrolides have limited activity against H. influenzae. Occasional isolates are found with higher macrolide MICs than those of baseline strains. The purpose of this study was to determine the changes that lead to such macrolide resistance in clinical strains of H. influenzae. Materials and methods. Clinical strains of H. influenzae used in this study were collected within the Alexander Project during 1997-2000. Macrolide resistant strains, defined as isolates with Azi MICs of >4 ug/ml or Cla MICs of >16 ug/ml, were studied for the presence of genes conferring resistance to macrolides and mutations in the genes coding for 23S rRNA, and L4 and L22 ribosomal proteins in H influenzae. Results. Among 6, 382 isolates screened prevalence of azithromycin and clarithromycin resistance was 1.3% and 2.8% respectively. A total of 43 macrolide non- susceptible strains studied for mechanism of resistance. No acquired macrolide resistance (erm, mef) genes were detected. From genomic sequence analysis it was found that 10 strains had L4 ribosomal protein mutations (63GT insertion, K61Q, T64K, G65D or D139G substitution), 11 had L22 ribosomal protein mutations (G91D substitution, 77DEGPSM insertion, 88RAKG insertion, 81S, 95RI or 96ILK deletion) and 7 had 23S ribosomal RNA A2058G, G2160U, G2161A, A2162U, or C2164G, base substitutions. One strain with G65D mutation in L4 had a raised MIC to Cla (32 ug/ml) but not to Azi (4 ug/ml).

Izvorni jezik
Engleski

Znanstvena područja
Temeljne medicinske znanosti



POVEZANOST RADA


Profili:

Avatar Url Mihaela Perić (autor)


Citiraj ovu publikaciju:

Bozdogan, Bulent; Peric, Mihaela; Jacobs, Michael R; Appelbaum, Peter C.
Macrolide hyper-susceptibility is associated with the abscence of efflux mechanism in clinical isolates of H. influenzae // 42nd ICAAC Abstracts, ASM
San Diego (CA), Sjedinjene Američke Države: ASM, 2002. str. 76-76 (poster, međunarodna recenzija, sažetak, znanstveni)
Bozdogan, B., Peric, M., Jacobs, M. & Appelbaum, P. (2002) Macrolide hyper-susceptibility is associated with the abscence of efflux mechanism in clinical isolates of H. influenzae. U: 42nd ICAAC Abstracts, ASM.
@article{article, author = {Bozdogan, Bulent and Peric, Mihaela and Jacobs, Michael R and Appelbaum, Peter C.}, year = {2002}, pages = {76-76}, keywords = {macrolide, susceptibility, H. Influenzae}, title = {Macrolide hyper-susceptibility is associated with the abscence of efflux mechanism in clinical isolates of H. influenzae}, keyword = {macrolide, susceptibility, H. Influenzae}, publisher = {ASM}, publisherplace = {San Diego (CA), Sjedinjene Ameri\v{c}ke Dr\v{z}ave} }
@article{article, author = {Bozdogan, Bulent and Peric, Mihaela and Jacobs, Michael R and Appelbaum, Peter C.}, year = {2002}, pages = {76-76}, keywords = {macrolide, susceptibility, H. Influenzae}, title = {Macrolide hyper-susceptibility is associated with the abscence of efflux mechanism in clinical isolates of H. influenzae}, keyword = {macrolide, susceptibility, H. Influenzae}, publisher = {ASM}, publisherplace = {San Diego (CA), Sjedinjene Ameri\v{c}ke Dr\v{z}ave} }




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