**1. Introduction**

The persistence and the resistance of *Escherichia coli* O157:H7 to disinfection are associated with its ability to form biofilms on food contact surfaces. Biofilms are communities of microorganisms embedded in an aqueous matrix of extracellular polymeric substances (EPS) produced by the attached cells; EPS are mainly composed by polysaccharides, proteins, lipids, and nucleic acids, which can vary in composition among strains and environmental conditions [1]. The adhesion and the biofilm formation of *E. coli* on food contact surfaces causes cross-contamination, and its consequences are observed on continuous outbreaks every year [2]. It has been reported that *E. coli* O157:H7 biofilms on stainless steel can lead to the release of embedded cells to contaminate other surfaces [3]. This information highlights the importance of studying the characteristics of *E. coli* biofilms to assure effective disinfection procedures.

Exopolysaccharides are secreted during *E. coli* O157:H7 biofilm development, and some of them include cellulose, colanic acid, and the adhesin poly-β-1,6-N-acetyl-glucosamine, and these polymers are involved in the maintenance of biofilm structure and cellular protection against disinfectants [4]. It has been reported that cellulose is the major EPS component of *E. coli* biofilms, and it is essential for its structure and strength, creating cell–cell and cell–surface interactions, retaining water, and avoiding the effect of disinfectants [5]. Previously it was demonstrated that degradation of the EPS matrix of *E. coli* O157:H7 biofilms (mainly composed by glucans) increased their susceptibility to disinfectants. The synthesis and the secretion of glucans are carried out by the enzyme glucosyltransferase, consisting of three transmembrane proteins (BcsA, BcsB, and BcsC) [6]. BcsA is the catalytically active subunit located within the cell, and it is responsible for the uridine diphosphate glucose (UDP-glucose) condensation, then the product is transferred to BcsB and BcsC subunits for processing and extracellular secretion [6]. Thus, blocking this enzymatic process could lead to the inhibition of biofilm production, leaving planktonic *E. coli* more susceptible to disinfectants.

The essential oil (EO) of lemongrass (*Cymbopogon citratus*) is rich in terpenes such as citral (85%) and geraniol (1.5%). *C. citratus* EO has been effective in inhibiting the planktonic growth of *E. coli* O157:H7 with a minimal inhibitory concentration (MIC) of 0.63 mg/mL [7], while Singh et al. [8] reported an MIC value of 0.008 mg/mL. On the other hand, citral and geraniol also showed antibacterial activity against *E. coli* as well as anti-quorum sensing activity at concentrations of 0.01 and 0.06 mg/mL, respectively [9]. On the other hand, *C. citratus* EO in combination with *Allium cepa* EO reduced the presence of *E. coli* in lettuce and spinach [10]. However, its antibacterial activity on planktonic cells could differ from the expected response against biofilms. In addition, *C. citratus* EO was able to inhibit *Staphylococcus aureus* and *Streptococcus mutans* biofilms [11,12]. Previous evidence described the ability of citral and geraniol-like terpenes to traverse the bacterial membrane and interact with vital metabolic enzymes [13]. Previous studies also evidenced the potential of citral to inactivate several enzymes [14,15]. Therefore, the objective of this study was to explore the effect of *C. citratus* EO, citral, and geraniol on the glucans production, glucosyltransferase activity, and biofilm formation of *E. coli* O157:H7.
