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

• Published in: Scientific reports Vol. 7; no. 1; pp. 5733 - 12
• Main Authors: Hashem, Yomna A., Amin, Heba M., Essam, Tamer M., Yassin, Aymen S., Aziz, Ramy K.
• Format: Journal Article
• Language: English
• Published: London Nature Publishing Group UK 18-07-2017; Nature Publishing Group; Nature Portfolio
• Subjects: 13; 45; 45/77; 631/326/41/2530; 631/326/46; Anti-Bacterial Agents - pharmacology; Antibiotic resistance; Antibiotics; Biofilms; Biofilms - drug effects; Biofilms - growth & development; Clinical isolates; Egypt; Enterococcus - drug effects; Enterococcus - genetics; Enterococcus - isolation & purification; Enterococcus - physiology; Gelatinase; Gene distribution; Genes, Bacterial; Genetic Association Studies; Genomes; Genotype; Gram-Positive Bacterial Infections - microbiology; Hospitals; Humanities and Social Sciences; Humans; multidisciplinary; Nosocomial infection; Polymerase Chain Reaction; Science; Science (multidisciplinary); Vancomycin; Vancomycin - pharmacology; Virulence; Virulence Factors - genetics; Egypt
• ISSN: 2045-2322; 2045-2322
• DOI: 10.1038/s41598-017-05901-0

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.