Acinetobacter baumannii, a microorganism with a worldwide epidemic spread, causes a wide range of infections, including pneumonia and blood-stream infections. This increasing threat in hospitals is mainly due to the occurrence of multidrug-resistant strains, associated with the real problem of eradication in the hospital wards . Biofilm formation may facilitate the environmental survival of A. baumannii by conferring resistance to antibiotics, desiccation or nutritional stress and explain the success of particular strains in hospitals [2, 3]. Several factors have been proved to play a role in this biofilm formation or maturation, like the poly-β-(1–6)-N-acetyl glucosamine extracellular polysaccharide, the biofilm-associated protein, the autotransporter Ata or the systems of protein glycosylation [4–7]. In addition, extracellular appendages are often involved in different stages of bacterial biofilm  as exemplified by the csuA/BABCDE chaperon-usher system, coding for fimbriae, and required for initial steps of A. baumannii biofilm development [6, 9, 10]. Recent findings have also demonstrated that more than one cell surface appendages system may be involved in the maintenance of the biofilm structure, especially when the biofilm is formed at the air-liquid interface . Finally, the presence of a type IV pili system and its involvement in motility was recently described in A. baumannii. It could also play a role in biofilm development (initial adhesion, microcolonies formation and in maturation, last step of biofilm formation) as demonstrated for other bacterial species [8, 13]. Therefore, the contribution of extracellular appendages to the biofilm structuration makes them very attractive as therapeutic targets .
In this study, we experienced this new approach by testing the use of the chemical agent virstatin. This small organic molecule has been demonstrated to inhibit Vibrio cholerae virulence and its orogastric administration would protect infant mice from V. cholerae intestinal colonization [15, 16]. Virstatin acted in preventing expression of the two major Vibrio cholerae virulence factors, cholera toxin and the toxin coregulated pilus (a type IV pilus, T4P). It would disrupt protein-protein interactions, i.e. the dimerization of the transcriptional regulator ToxT, stopping thus the activation of ctx and tcp genes [15, 16].
We present here the efficacy of the virstatin as an inhibitor of the pili system synthesis to prevent A. baumannii biofilm formation.