Aims: Pseudomonas aeruginosa is a drug resistance opportunistic bacterium. Biofilm formation is key factor for survival of P. aeruginosa in various environments. Polysaccharides may be involved in biofilm formation. The purpose of this study was to evaluate antimicrobial and anti-biofilm activities of seven plant extracts with known alpha-glucosidase inhibitory activities on different strains of P. aeruginosa. Methodology and results: Plants were extracted with methanol by the maceration method. Antimicrobial activities were determined by agar dilution and by growth yield as measured by OD560nm of the Luria Bertani broth (LB) culture with or without extracts. In agar dilution method, extracts of Quercus infectoria inhibited the growth of all, while Myrtus communis extract inhibited the growth of 3 out of 8 bacterial strains with minimum inhibitory concentration (MIC) of 1000 μg/mL. All extracts significantly (p≤0.003) reduced growth rate of the bacteria in comparison with the control without extracts in LB broth at sub-MIC concentrations (500 μg/mL). All plant extracts significantly (p≤0.003) reduced biofilm formation compared to the controls. Glycyrrhiza glabra and Q. infectoria had the highest anti-biofilm activities. No correlation between the alpha-glucosidase inhibitory activity with growth or the intensity of biofilm formation was found. Conclusion, significance and impact of study: Extracts of Q. infectoria and M. communis had the most antimicrobial, while Q. infectoria and G. glabra had the highest anti-biofilm activities. All plant extracts had anti-biofilm activities with marginal effect on growth, suggesting that the mechanisms of these activities are unrelated to static or cidal effects. Further work to understand the relation between antimicrobial and biofilm formation is needed for development of new means to fight the infectious caused by this bacterium in future.

BACKGROUND: Enterococcus faecalis is an opportunistic pathogen that causes most of the enterococcal infections. Among the different factors implicated in the pathogenesis of these organisms, biofilm formation and antibiotic resistance are the most important. The ability for biofilm formation has been attributed to the presence of some virulence genes. However, no definite correlation has been found. This study aimed to detect biofilm formation and antibiotic resistance patterns in E. faecalis isolates collected from clinical and fecal samples, and to investigate possible correlation between some virulence genes (esp, cyl, gelE) and biofilm formation. MATERIALS AND METHODS: A collection of 123 E. faecalis isolates were investigated for antibiotic resistance and production of hemolysin, gelatinase, and biofilm using phenotypic methods. The esp, gelE and cyl genes were detected using polymerase chain reaction. RESULTS: Thirty-eight pathogenic isolates (37%) were positive for biofilm formation. Additionally, the gelE, esp, and cyl genes were detected in 74 (71.8%), 79 (76.7%) and 42 (40.8%) isolates, respectively. In the fecal samples, 18 (90%) isolates were biofilm producers and 11 (55%), 17 (85%) and 8 (40%) isolates were positive for gelE, esp, and cyl, respectively. There were significant differences in biofilm production between pathogenic and fecal isolates (P <0.001). Multidrug resistance (MDR) was found among 32% (n = 33) and 15% (n = 3) of the clinical and fecal isolates, respectively. However, no significant difference was seen between MDR and biofilm formation. Five pathogenic and two fecal isolates were negative for all investigated genes while they were they were biofilm producers. In contrast, 22 pathogenic isolates and 1 fecal isolate were positive for the tested genes, but did not form any biofilm. No significant differences were observed between biofilm formation and the presence of the esp, gelE and cyl genes in the pathogenic and fecal isolates (P ˃0.05). CONCLUSION: The presence of the esp, gelE and cyl genes might not be determining factors for biofilm formation in enterococci and other mechanisms might be involved in this process.
Biofilms* ; Drug Resistance, Microbial ; Drug Resistance, Multiple ; Enterococcus faecalis* ; Enterococcus* ; Gelatinases ; Polymerase Chain Reaction ; Virulence*