## 1 Introduction  
Cholera infection caused by the Gram-negative, aquatic bacterium _Vibrio cholerae_ leads to severe dehydrating diarrhea [1]. The worldwide spread of _V. cholerae_ has caused seven large pandemic events in recorded history and remains a serious threat to public health in developing countries [2, 3]. Approximately 2 to 9 million cases of cholera occur annually, resulting in near 100,000 deaths [4]. The case-fatality ratio is correlated mainly with proper and rapid treatment, ranging from 15.8% to less than 1%, according to WHO statistics. Currently, the antibiotic resistance among _V. cholerae_ strains is increasingly reported and threatens our ability to treat infected patients--which has created a major challenge to the development of an efficient therapy [5, 6, 7]. Oral rehydration treatment (ORT) is still the first-choice therapy for infected patients [8]. In more serious cases, intravenous rehydration and antibiotics are employed to reduce severe complication development. However, the ORT helps only to reduce symptoms of infection instead of actual treatment and cannot eliminate the cause of dysentery, while the continuous use of antibiotics contributes to a rapid emergence of antibiotic-resistant strains. Cholera toxin (CT) and the toxin coregulated pilus (TCP) are two major virulence factors responsible for toxigenic abilities and intestinal colonization, respectively. Toxicenic abilities of _V. cholerae_ are a consequence of CT synthesis encoded by the _ctxAB_ gene, located on the CTX prophage integrated on the main chromosome. This has prompted many researchers to investigate the therapeutic potentials of traditional foods and beverages as well as natural products to inhibit the growth of _V. cholerae_ or secretion of CT [5; 9]. Moreover, virulence factors are regulated at the transcriptional level by a coordinated network of proteins that respond to specific environmental signals. Among these proteins is ToxT, an AraC family regulator that binds the promoters _tcpA_ and _ctx_ and directly activates virulence gene expression [1]. ToxT plays an essential role in _V. cholerae_ virulence, and its expression and activity are highly regulated among epidemic _V. cholerae_ strains. _V. cholerae_ strains are a common bacterial flora found in their natural reservoirs, both in freshwater and marine environments [10]. In these conditions, _V. cholerae_ is mainly attached to the biotic surfaces, including those of aquatic species such as plankton, clams, crustaceans, plants, and insects [10; 11]. The efficient propagation and resistance of bacterial cells in a nutritionally poor aquatic environment is facilitated by biofilm formation. It is assumed that the bacteria existing in the biofilm show a reduced sensitivity to environmental stresses, including digestion in the gastrointestinal tract, which is a route of infection; thus, the ability to form and maintain a biofilm is of serious clinical importance. Growth in biofilm induces a hyper-infectious phenotype in _V. cholerae_[12]; hence this feature and generally the higher number of bacteria in biofilm play a key role in transmission [13; 14]. The hyperinfective state refers to a decrease in the number of cells required to cause disease. Thus, biofilm prevention and eradication are crucial steps in an anti-cholerae strategy. In an ongoing challenging era where microbial resistance to antibiotics is a significant problem in controlling infections caused by bacteria and in the occurrence of recurrent epidemics due to drug-resistant microorganisms, the development of new therapeutic strategies is of high priority. Targeting the regulation of bacterial virulence is considered one of the promising approaches [14; 15]. Current antimicrobials in their mode of action target a relatively small number of essential cell functions such as DNA/RNA, cell wall, or protein synthesis. So, if these global process inhibitors are no longer effective, extensive efforts should be undertaken to investigate new and more specific targets.