EFFECT OF PHENOLIC COMPOUNDS ON Staphylococcus aureus BIOFILM DEVELOPMENT

A LOMBARTE SERRAT; C DOTTO; M HRAST; M SOVA; S GOBEC; M SULIGOY; D SORDELLI; L SASO; M GIACOMODONATO, ; F BUZZOLA

Cordoba

Congreso; XI Congreso Argentino de Microbiología General - SAMIGE 2015; 2015

Sociedad Argentina de Microbiología General - SAMIGE

Staphylococcus aureus causes a wide range infectious diseases in humans and animals. Biofilms have been linked to bovine mastitis since S. aureus biofilm-producer strains showed an increased ability to attach to mammary mucosal surfaces and cause persistent infections compared with non-biofilm forming strains. S. aureus biofilm formation partially depends upon the production of polysaccharide intercellular adhesin (PIA), coded by the ica operon. Antibiotic therapy is becoming increasingly ineffective in the treatment of biofilm-associated infections. Therefore, the search for new chemical compounds with anti-biofilm properties becomes necessary. The aim of this study was to investigate the inhibitory effect of four phenolic compounds (named F1-F4 for simplicity) prior-to and post- biofilm formation by S. aureus. To avoid the identification of strain-specific hits, the study was performed on five S. aureus isolates from milk of bovines with mastitis and two laboratory reference (Newman and SA113) S. aureus strains. The isolates were selected for their ability to produce large amounts of biofilm by either ica-dependent or -independent mechanisms. Bacteria were treated with compounds before biofilm formation takes place (prior-to-exposure) and 24 h after biofilms were formed (post-exposure). The biofilm biomass was stained with crystal violet for spectrophotometric quantification. The initial screening in the Newman strain allowed to classify the phenolic compounds as inactive (F1), moderately active (F2, F4) or highly active (F3). Only N-(3-cyano-4,5,6,7-tetrahydrobenzo[b]thiophen-2-yl)-3-hydroxybenzamide (F3) presented a moderate but significant dose-dependent effect on the inhibition of biofilm formed by the strains under study. The different phenolic compounds showed no bacteriostatic or bactericidal activity. The prior-to-exposure evaluation revealed that F2 induced 89%, 86% and 43% biofilm inhibition in AR99, RF122 and SA113 S. aureus strains, respectively. F3 was able to inhibit by 77% to 23% the biofilm formation in all strains under scrutiny except AR77. F4 decreased biofilm production by 23% only in the Newman strain. No compound affected the AR77 biofilm formation. Results obtained by post-exposure of phenolic compounds indicated that F3 showed an anti-biofilm effect in most strains analyzed except V329 and RF122. Data obtained from F1 experiments did not show any significant effect on biofilm inhibition or inactivation in any of the strains under study confirming its inactivity. It is likely that in the presence of F3, certain bacterial cells are able to attach and form biofilms, but their maturation process is significantly hampered. This study highlights the potential of F3 as a successful agent that can act prior-to and post- biofilm development.