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.
Highlights
Enterococci are nosocomial pathogens that can form biofilms, which contribute to their virulence and antibiotic resistance
We found that agg is a good predictor of biofilm strength, that the fsrA and fsrB genes have a high predictive value of biofilm-associated gelatinase activity, and that sub-minimal inhibitory concentrations of vancomycin were able to inhibit biofilm formation
Because the genomic survey we performed on ~190 genomes (Table S2), as well as our polymerase chain reaction (PCR) results (Table 3), indicated that fsrB is more frequent than fsrA, and that no cases were found in which fsrA was present in absence of fsrB, we suggest that fsrB is sufficient to predict the gelatinase activity (Chi-Square P value = 0.0012, Table 5)
Summary
Enterococci are nosocomial pathogens that can form biofilms, which contribute to their virulence and antibiotic resistance. Biofilm formation is associated with quorum sensing, which is the regulation of bacterial gene expression in response to large cell population densities. In E. faecalis, biofilm formation is regulated by the well-defined quorum sensing system, fsr (faecal streptococci regulator) locus[11] This locus consists of three genes, fsrA, fsrB and fsrC, immediately located next to two virulence factor-encoding genes: one encoding a gelatinase (gelE) and the other a serine protease (sprE). Enterococcal cells do communicate through Fsr quorum signaling, but are capable of communicating by peptide pheromones, secreted by recipient cells to induce the conjugative apparatus of donor cell, which mediate the transfer of pheromone-responsive plasmids[13] Some of these plasmids carry genes that regulate or promote biofilm formation, such as the plasmid-encoded aggregation substance genes[14]. Examples of secreted enterococcal pheromones are Cpd, Cob, and Ccf[16]
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