“
“Background Stenotrophomonas maltophilia is a Gram-negative opportunistic pathogen in hospitalized or compromised patients [1, 2]. In the last decade, it has emerged as one of the most frequently found bacteria in cystic fibrosis (CF) patients [3, 4]. However, the role of this opportunistic pathogen as an innocent bystander or causative agent often remains unclear [5, 6] and little is known about its virulence factors [7–9]. Biofilms, sessile structured bacterial communities exhibiting recalcitrance to antimicrobial compounds Entospletinib and persistence despite sustained host defenses, are increasingly recognized as a contributing

factor to disease pathogenesis in CF and other respiratory tract diseases associated with chronic bacterial infections [10, 11]. While S. maltophilia CF isolates are known to have the ability to form biofilms on both abiotic surfaces [12–16] and CF-derived epithelial monolayer [17], it is not clear whether there is an intrinsic difference in biofilm formation among genomically diverse environmental and clinical isolates of S. maltophilia. The molecular mechanisms underlying biofilm formation in S. maltophilia have not been extensively studied. Recently, mutants for the glucose-1-phosphate thymidyltransferase rmlA gene and for the cis-11-methyl-2-dodecenoic

acid rpfF gene are reported to decrease biofilm formation [18, 19]. Further, the spgM gene, encoding a bifunctional enzyme with both phosphoglucomutase (PGM) and phosphomannomutase activities, could be involved in biofilm-forming ability because of the homology with the algC gene Syk inhibitor that is responsible for the production of a PGM associated with LPS and alginate biosynthesis in P. aeruginosa [20]. Several P5091 datasheet typing schemes have been used successfully in the molecular selleck kinase inhibitor epidemiology of S. maltophilia strains in an attempt to investigate the epidemiology of infections and nosocomial outbreaks caused by this microorganism. Phenotypic methods – such as serotyping, antibiotyping and biotyping – have proven to be poorly discriminative because of a low interstrain variability

[21]. Molecular typing techniques have been successfully used to study the epidemiology of S. maltophilia revealing a genetically high diversity in this species [21–26]. In this study, we examined a set of 98 isolates of S. maltophilia – obtained from clinical (CF and non-CF patients) and environmental sources – for phenotypic (biofilm formation, mean generation time, swimming and twitching motilities, susceptibility to oxidative stress) and genotypic (clonal relatedness) traits in order to find significant differences among the groups considered. In addition, the relationship between biofilm production and the detection of rmlA, spgM, and rpfF genes was evaluated. Virulence was also assessed by using an experimental model of airborne lung infection. Our results indicate that CF S.