EFFECT OF PHENOLIC COMPOUNDS ON Staphylococcus aureus BIOFILM DEVELOPMENT.

LOMBARTE SERRAT ANDREA; DOTTO CRISTIAN; HRAST MARTINA; SOVA MATEJ; GOBEC STANISLAV; SULIGOY MAURICIO; SORDELLI DANIEL; SASO LUCIANO; GIACOMODONATO MONICA; BUZZOLA FERNANDA

Córdoba

Congreso; SAMIGE XI; 2015

Staphylococcus aureus causes a wide range infectious diseases in humans and animals. Biofilmshave been linked to bovine mastitis since S. aureus biofilm-producer strains showed an increasedability to attach to mammary mucosal surfaces and cause persistent infections compared withnon-biofilm forming strains. S. aureus biofilm formation partially depends upon the production ofpolysaccharide intercellular adhesin (PIA), coded by the ica operon. Antibiotic therapy is becomingincreasingly ineffective in the treatment of biofilm-associated infections. Therefore, the search for newchemical compounds with anti-biofilm properties becomes necessary. The aim of this study was toinvestigate the inhibitory effect of four phenolic compounds (named F1-F4 for simplicity) prior-to andpost- biofilm formation by S. aureus. To avoid the identification of strain-specific hits, the study wasperformed 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 largeamounts of biofilm by either ica-dependent or -independent mechanisms. Bacteria were treated withcompounds before biofilm formation takes place (prior-to-exposure) and 24 h after biofilms wereformed (post-exposure). The biofilm biomass was stained with crystal violet for spectrophotometricquantification. The initial screening in the Newman strain allowed to classify the phenolic compoundsas inactive (F1), moderately active (F2, F4) or highly active (F3). OnlyN-(3-cyano-4,5,6,7-tetrahydrobenzo[b]thiophen-2-yl)-3-hydroxybenzamide (F3) presented a moderatebut significant dose-dependent effect on the inhibition of biofilm formed by the strains under study. Thedifferent phenolic compounds showed no bacteriostatic or bactericidal activity. The prior-to-exposureevaluation revealed that F2 induced 89%, 86% and 43% biofilm inhibition in AR99, RF122 and SA113S. aureus strains, respectively. F3 was able to inhibit by 77% to 23% the biofilm formation in all strainsunder scrutiny except AR77. F4 decreased biofilm production by 23% only in the Newman strain. Nocompound affected the AR77 biofilm formation. Results obtained by post-exposure of phenoliccompounds indicated that F3 showed an anti-biofilm effect in most strains analyzed except V329 andRF122. Data obtained from F1 experiments did not show any significant effect on biofilm inhibition orinactivation in any of the strains under study confirming its inactivity. It is likely that in the presence ofF3, certain bacterial cells are able to attach and form biofilms, but their maturation process issignificantly hampered. This study highlights the potential of F3 as a successful agent that can actprior-to and post- biofilm development.