Biofilm formation in enterococci: genotype-phenotype correlations and inhibition by vancomycin

Abstract Enterococci are nosocomial pathogens that can form biofilms, which contribute to their virulence and antibiotic resistance. Although many genes involved in biofilm formation have been defined, their distribution among enterococci has not been comprehensively studied on a genome scale, and t...

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Autores principales:	Yomna A. Hashem, Heba M. Amin, Tamer M. Essam, Aymen S. Yassin, Ramy K. Aziz
Formato:	article
Lenguaje:	EN
Publicado:	Nature Portfolio 2017
Materias:	Medicine R Science Q
Acceso en línea:	https://doaj.org/article/b4da75bbb99248f987982e90dbc1fca1
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spelling	oai:doaj.org-article:b4da75bbb99248f987982e90dbc1fca12021-12-02T11:52:35ZBiofilm formation in enterococci: genotype-phenotype correlations and inhibition by vancomycin10.1038/s41598-017-05901-02045-2322https://doaj.org/article/b4da75bbb99248f987982e90dbc1fca12017-07-01T00:00:00Zhttps://doi.org/10.1038/s41598-017-05901-0https://doaj.org/toc/2045-2322Abstract Enterococci are nosocomial pathogens that can form biofilms, which contribute to their virulence and antibiotic resistance. Although many genes involved in biofilm formation have been defined, their distribution among enterococci has not been comprehensively studied on a genome scale, and their diagnostic ability to predict biofilm phenotypes is not fully established. Here, we assessed the biofilm-forming ability of 90 enterococcal clinical isolates. Major patterns of virulence gene distribution in enterococcal genomes were identified, and the differentiating virulence genes were screened by polymerase chain reaction (PCR) in 31 of the clinical isolates. We found that detection of gelE in Enterococcus faecalis is not sufficient to predict gelatinase activity unless fsrAB, or fsrB alone, is PCR-positive (P = 0.0026 and 0.0012, respectively). We also found that agg is significantly enriched in isolates with medium and strong biofilm formation ability (P = 0.0026). Additionally, vancomycin, applied at sub minimal inhibitory concentrations, inhibited biofilm in four out of five strong biofilm-forming isolates. In conclusion, we suggest using agg and fsrB genes, together with the previously established gelE, for better prediction of biofilm strength and gelatinase activity, respectively. Future studies should explore the mechanism of biofilm inhibition by vancomycin and its possible use for antivirulence therapy.Yomna A. HashemHeba M. AminTamer M. EssamAymen S. YassinRamy K. AzizNature PortfolioarticleMedicineRScienceQENScientific Reports, Vol 7, Iss 1, Pp 1-12 (2017)
institution	DOAJ
collection	DOAJ
language	EN
topic	Medicine R Science Q
spellingShingle	Medicine R Science Q Yomna A. Hashem Heba M. Amin Tamer M. Essam Aymen S. Yassin Ramy K. Aziz Biofilm formation in enterococci: genotype-phenotype correlations and inhibition by vancomycin
description	Abstract Enterococci are nosocomial pathogens that can form biofilms, which contribute to their virulence and antibiotic resistance. Although many genes involved in biofilm formation have been defined, their distribution among enterococci has not been comprehensively studied on a genome scale, and their diagnostic ability to predict biofilm phenotypes is not fully established. Here, we assessed the biofilm-forming ability of 90 enterococcal clinical isolates. Major patterns of virulence gene distribution in enterococcal genomes were identified, and the differentiating virulence genes were screened by polymerase chain reaction (PCR) in 31 of the clinical isolates. We found that detection of gelE in Enterococcus faecalis is not sufficient to predict gelatinase activity unless fsrAB, or fsrB alone, is PCR-positive (P = 0.0026 and 0.0012, respectively). We also found that agg is significantly enriched in isolates with medium and strong biofilm formation ability (P = 0.0026). Additionally, vancomycin, applied at sub minimal inhibitory concentrations, inhibited biofilm in four out of five strong biofilm-forming isolates. In conclusion, we suggest using agg and fsrB genes, together with the previously established gelE, for better prediction of biofilm strength and gelatinase activity, respectively. Future studies should explore the mechanism of biofilm inhibition by vancomycin and its possible use for antivirulence therapy.
format	article
author	Yomna A. Hashem Heba M. Amin Tamer M. Essam Aymen S. Yassin Ramy K. Aziz
author_facet	Yomna A. Hashem Heba M. Amin Tamer M. Essam Aymen S. Yassin Ramy K. Aziz
author_sort	Yomna A. Hashem
title	Biofilm formation in enterococci: genotype-phenotype correlations and inhibition by vancomycin
title_short	Biofilm formation in enterococci: genotype-phenotype correlations and inhibition by vancomycin
title_full	Biofilm formation in enterococci: genotype-phenotype correlations and inhibition by vancomycin
title_fullStr	Biofilm formation in enterococci: genotype-phenotype correlations and inhibition by vancomycin
title_full_unstemmed	Biofilm formation in enterococci: genotype-phenotype correlations and inhibition by vancomycin
title_sort	biofilm formation in enterococci: genotype-phenotype correlations and inhibition by vancomycin
publisher	Nature Portfolio
publishDate	2017
url	https://doaj.org/article/b4da75bbb99248f987982e90dbc1fca1
work_keys_str_mv	AT yomnaahashem biofilmformationinenterococcigenotypephenotypecorrelationsandinhibitionbyvancomycin AT hebamamin biofilmformationinenterococcigenotypephenotypecorrelationsandinhibitionbyvancomycin AT tamermessam biofilmformationinenterococcigenotypephenotypecorrelationsandinhibitionbyvancomycin AT aymensyassin biofilmformationinenterococcigenotypephenotypecorrelationsandinhibitionbyvancomycin AT ramykaziz biofilmformationinenterococcigenotypephenotypecorrelationsandinhibitionbyvancomycin
_version_	1718395006522228736

Biofilm formation in enterococci: genotype-phenotype correlations and inhibition by vancomycin

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