Plasmid curing was used to examine the function of plasmids. Five plasmids of A. Protein Tyrosine Kinase inhibitor baumannii A3 were cured but no differences were observed between wild-type and plasmid-cured strains with respect to the biofilm formation capabilities. The prevalence of A. baumannii strains with biofilm mode of growth could explain their ability to persist in clinical environments and their role in device-related infections. The genus Acinetobacter includes a group of bacteria that are nonmotile, Gram-negative coccobacilli, displaying strict aerobic metabolism.
Acinetobacter spp. have evolved as important nosocomial pathogens. They are found in diverse environments such as soil, water, food products and are often isolated from medical devices (Bergogne-Bérézin & Towner, 1996). They cause severe infections in immune-compromised patients by colonizing on different medical
devices and surviving on these surfaces (Tomaras et al., 2003). A large number of reports describe the outbreaks of Acinetobacter-associated nosocomial infections such as secondary meningitis, pneumonia, wound, burn and urinary tract infections (UTI) (Bergogne-Berenzin et al., 1993; Patwardhan et al., 2008). Biofilm formation Autophagy activity is an important feature of most clinical isolates of Acinetobacter spp. Biofilms are assemblages of surface microbial cells that are enclosed in an extracellular polymeric matrix (Donlan, 2002). It is clear from the epidemiologic evidence that Acinetobacter biofilms play a role in infectious diseases such Thiamet G as cystic fibrosis, periodontitis, in bloodstream and UTI because of their ability to indwell
medical devices (Struelens et al., 1993; Donlan & Costerton, 2002; Gaddy et al., 2009). Acinetobacter is known to show resistance to a majority of commercially available antibiotics (penicillins, aminoglycosides, cephalosporins, quinolones) and therefore raises an important therapeutic problem (Smolyakov et al., 2004; Shin et al., 2009). A control of the spread of these infections thus demands the removal of Acinetobacter spp. from medical settings (Zavascki et al., 2010). Antibiotic resistance markers are often plasmid borne and plasmids present in Acinetobacter strains can be transferred to other pathogenic bacteria (Chopade et al., 1985; Patwardhan et al., 2008). The ability of Acinetobacter species to adhere to the surfaces, form biofilms, display antibiotic resistance and gene transfer means that there is an urgent need to study the factors responsible for their spread. In the present study, biofilm formation on different abiotic surfaces by six clinical isolates of Acinetobacter baumannii obtained from UTI, as well as catheter surfaces, and the effects of physical parameters (temperature, pH and NaCl) on biofilm formation, was investigated. Factors such as cell surface hydrophobicity (CSH) and production of lectins, important in biofilm formation, were also evaluated.