Distribution of erm genes and low prevalence of inducible resistance to clindamycin among staphylococci isolates

Detalhes bibliográficos
Autor(a) principal: Coutinho, Vivian de Lima Spode
Data de Publicação: 2010
Outros Autores: Paiva, Rodrigo Minuto, Reiter, Keli Cristine, Paris, Fernanda de, Barth, Afonso Luis, Machado, Alice Beatriz Mombach Pinheiro
Tipo de documento: Artigo
Idioma: eng
Título da fonte: Repositório Institucional da UFRGS
Texto Completo: http://hdl.handle.net/10183/87955
Resumo: Introduction: Resistance to macrolides, lincosamides and streptogramins B (MLSB antibiotics) in staphylococci may be due to modification in ribosomal target methylase encoded by erm genes. The expression of MLSB resistance lead to three phenotypes, namely constitutive resistance (cMLSB), inducible resistance (iMLSB), and resistance only to macrolides and streptogramins B (MSB). The iMLSB resistance is the most difficult to detect in the clinical laboratory. Objective: This study investigated the expression of MLSB resistance and the prevalence of the erm genes among 152 clinical isolates of Staphylococcus aureus and coagulase-negative Staphylococcus (CNS) from Hospital de Clínicas de Porto Alegre. Methods: Primary MLSB resistance was detected by the disk diffusion method. Isolates with iMLSB phenotype were tested by double-disk induction method. All isolates were tested by a genotypic assay, PCR with specific primers. Results: A total of 46.7% of staphylococci were positive for cMLSB; 3.3% for iMLSB and 3.3% for MSB. One or more erm genes were present in 50.1% of isolates. The gene ermA was detected in 49 isolates, ermC in 29 and ermB in 3. Conclusion: The prevalence of the ermA, ermB and ermC genes were 29.6%, 17.1% and 0.66% respectively, and constitutive resistance was the most frequent as compared to the other two phenotypes.
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spelling Coutinho, Vivian de Lima SpodePaiva, Rodrigo MinutoReiter, Keli CristineParis, Fernanda deBarth, Afonso LuisMachado, Alice Beatriz Mombach Pinheiro2014-02-28T01:50:33Z20101413-8670http://hdl.handle.net/10183/87955000872523Introduction: Resistance to macrolides, lincosamides and streptogramins B (MLSB antibiotics) in staphylococci may be due to modification in ribosomal target methylase encoded by erm genes. The expression of MLSB resistance lead to three phenotypes, namely constitutive resistance (cMLSB), inducible resistance (iMLSB), and resistance only to macrolides and streptogramins B (MSB). The iMLSB resistance is the most difficult to detect in the clinical laboratory. Objective: This study investigated the expression of MLSB resistance and the prevalence of the erm genes among 152 clinical isolates of Staphylococcus aureus and coagulase-negative Staphylococcus (CNS) from Hospital de Clínicas de Porto Alegre. Methods: Primary MLSB resistance was detected by the disk diffusion method. Isolates with iMLSB phenotype were tested by double-disk induction method. All isolates were tested by a genotypic assay, PCR with specific primers. Results: A total of 46.7% of staphylococci were positive for cMLSB; 3.3% for iMLSB and 3.3% for MSB. One or more erm genes were present in 50.1% of isolates. The gene ermA was detected in 49 isolates, ermC in 29 and ermB in 3. Conclusion: The prevalence of the ermA, ermB and ermC genes were 29.6%, 17.1% and 0.66% respectively, and constitutive resistance was the most frequent as compared to the other two phenotypes.application/pdfengThe Brazilian journal of infectious diseases. Vol. 14, no. 6 (2010), p. 564-568MacrolídeosStaphylococcusEritromicinaerm genesmacrolidesresistanceStaphylococcusDistribution of erm genes and low prevalence of inducible resistance to clindamycin among staphylococci isolatesinfo:eu-repo/semantics/articleinfo:eu-repo/semantics/otherinfo:eu-repo/semantics/publishedVersioninfo:eu-repo/semantics/openAccessreponame:Repositório Institucional da UFRGSinstname:Universidade Federal do Rio Grande do Sul (UFRGS)instacron:UFRGSORIGINAL000872523.pdf000872523.pdfTexto completo (inglês)application/pdf854698http://www.lume.ufrgs.br/bitstream/10183/87955/1/000872523.pdf68fb40238e14ac7f4e25a86e057f008dMD51TEXT000872523.pdf.txt000872523.pdf.txtExtracted Texttext/plain22004http://www.lume.ufrgs.br/bitstream/10183/87955/2/000872523.pdf.txt98e9cc4b93ac610faff83df38917db9eMD52THUMBNAIL000872523.pdf.jpg000872523.pdf.jpgGenerated Thumbnailimage/jpeg1874http://www.lume.ufrgs.br/bitstream/10183/87955/3/000872523.pdf.jpg5c8d0379b7d87dd6f6e97e61ed5ec348MD5310183/879552023-06-15 03:27:56.571964oai:www.lume.ufrgs.br:10183/87955Repositório de PublicaçõesPUBhttps://lume.ufrgs.br/oai/requestopendoar:2023-06-15T06:27:56Repositório Institucional da UFRGS - Universidade Federal do Rio Grande do Sul (UFRGS)false
dc.title.pt_BR.fl_str_mv Distribution of erm genes and low prevalence of inducible resistance to clindamycin among staphylococci isolates
title Distribution of erm genes and low prevalence of inducible resistance to clindamycin among staphylococci isolates
spellingShingle Distribution of erm genes and low prevalence of inducible resistance to clindamycin among staphylococci isolates
Coutinho, Vivian de Lima Spode
Macrolídeos
Staphylococcus
Eritromicina
erm genes
macrolides
resistance
Staphylococcus
title_short Distribution of erm genes and low prevalence of inducible resistance to clindamycin among staphylococci isolates
title_full Distribution of erm genes and low prevalence of inducible resistance to clindamycin among staphylococci isolates
title_fullStr Distribution of erm genes and low prevalence of inducible resistance to clindamycin among staphylococci isolates
title_full_unstemmed Distribution of erm genes and low prevalence of inducible resistance to clindamycin among staphylococci isolates
title_sort Distribution of erm genes and low prevalence of inducible resistance to clindamycin among staphylococci isolates
author Coutinho, Vivian de Lima Spode
author_facet Coutinho, Vivian de Lima Spode
Paiva, Rodrigo Minuto
Reiter, Keli Cristine
Paris, Fernanda de
Barth, Afonso Luis
Machado, Alice Beatriz Mombach Pinheiro
author_role author
author2 Paiva, Rodrigo Minuto
Reiter, Keli Cristine
Paris, Fernanda de
Barth, Afonso Luis
Machado, Alice Beatriz Mombach Pinheiro
author2_role author
author
author
author
author
dc.contributor.author.fl_str_mv Coutinho, Vivian de Lima Spode
Paiva, Rodrigo Minuto
Reiter, Keli Cristine
Paris, Fernanda de
Barth, Afonso Luis
Machado, Alice Beatriz Mombach Pinheiro
dc.subject.por.fl_str_mv Macrolídeos
Staphylococcus
Eritromicina
topic Macrolídeos
Staphylococcus
Eritromicina
erm genes
macrolides
resistance
Staphylococcus
dc.subject.eng.fl_str_mv erm genes
macrolides
resistance
Staphylococcus
description Introduction: Resistance to macrolides, lincosamides and streptogramins B (MLSB antibiotics) in staphylococci may be due to modification in ribosomal target methylase encoded by erm genes. The expression of MLSB resistance lead to three phenotypes, namely constitutive resistance (cMLSB), inducible resistance (iMLSB), and resistance only to macrolides and streptogramins B (MSB). The iMLSB resistance is the most difficult to detect in the clinical laboratory. Objective: This study investigated the expression of MLSB resistance and the prevalence of the erm genes among 152 clinical isolates of Staphylococcus aureus and coagulase-negative Staphylococcus (CNS) from Hospital de Clínicas de Porto Alegre. Methods: Primary MLSB resistance was detected by the disk diffusion method. Isolates with iMLSB phenotype were tested by double-disk induction method. All isolates were tested by a genotypic assay, PCR with specific primers. Results: A total of 46.7% of staphylococci were positive for cMLSB; 3.3% for iMLSB and 3.3% for MSB. One or more erm genes were present in 50.1% of isolates. The gene ermA was detected in 49 isolates, ermC in 29 and ermB in 3. Conclusion: The prevalence of the ermA, ermB and ermC genes were 29.6%, 17.1% and 0.66% respectively, and constitutive resistance was the most frequent as compared to the other two phenotypes.
publishDate 2010
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dc.relation.ispartof.pt_BR.fl_str_mv The Brazilian journal of infectious diseases. Vol. 14, no. 6 (2010), p. 564-568
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