Abstract
Bacterial growth as a biofilm on solid surfaces is strongly associated with the development of human infections. Biofilms on native heart valves (infective endocarditis) is a life-threatening disease as a consequence of bacterial resistance to antimicrobials in such a state. Enterococci have emerged as a cause of endocarditis and nosocomial infections despite being normal commensals of the gastrointestinal and female genital tracts. We examined the role of two-component signal transduction systems in biofilm formation by theEnterococcus faecalisV583 clinical isolate and identified thefsrregulatory locus as the sole two-component system affecting this unique mode of bacterial growth. Insertion mutations in thefsroperon affected biofilm formation on two distinct abiotic surfaces. Inactivation of thefsr-controlled genegelEencoding the zinc-metalloprotease gelatinase was found to prevent biofilm formation, suggesting that this enzyme may present a unique target for therapeutic intervention in enterococcal endocarditis.

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