For instance, they are resistant to antimicrobial agents in comparison to planktonic cells [6–8]. As more than 65% of biofilms with human microbial infections are caused by biofilms [5], there is an urgent need to

understand biofilm behaviour. The genus 7-Cl-O-Nec1 datasheet Candida comprises more than 150 pathogenic and nonpathogenic yeast species. Among these, C. albicans, C. tropicalis, C. parapsilosis, C. krusei, C. kefyr, C. glabrata and C. guillermondii are recognized as medically important pathogens [9]. C. albicans is the most prevalent yeast isolated from humans (47-75%) followed by C. tropicalis (7%), C. glabrata (7%), C. krusei (5%), C. parapsilosis (< 5%) and C. guillermondii (< 5%) [9]. Common Candidal habitats of humans include the gut, skin and mucosal surfaces, while one half of the human population

carry Candida in their oral cavities[10]. Pseudomonas aeruginosa is an DZNeP concentration AZD5582 cell line aerobic Gram-negative bacterium that causes community acquired infections, such as ulcerative keratitis, otitis externa, skin and soft tissue infections and, nosocomial infections including pneumonias, urinary tract infections, infections in surgical sites and burns [24, 25]. Indeed, out of all nosocomial infections in different ethnic communities, 11-13.8% is found to be caused by P. aeruginosa [11–13]. United States Cystic Fibrosis Foundation Patients Registry (2004), has stated that 57.3% of all reported respiratory cultures contained P. aeruginosa indicating its important role in causing chronic and recurrent infections in cystic fibrotic patients [14]. Lee et al [15] have demonstrated that P. aeruginosa is the most commonly identified cause of septicemia in primary immunodeficiency and some 20% of bacteriaemia in acute leukemic patients [16, 17]. Incidence of P. aeruginosa bacteriaemias in HIV affected patients is approximately MRIP 10 times higher

than that of the normal population [18]. Pathogenic interactions between C. albicans and P. aeruginosa have recently been demonstrated by a number of groups [19, 20]. The antifungal behaviour of P. aeruginosa against Candida spp. was first reported in early nineties by Kerr et al [20]. Subsequently others have shown that P. aeruginosa kills C. albicans by forming a dense film on fungal filaments, though, it neither binds nor kills the yeast-form of C. albicans [19]. Thein et al [21] have also reported that P. aeruginosa ATCC 27853 at a concentration gradient elicited a significant inhibition of Candida albicans biofilms. Although, the structure and the properties of monospecies biofilms and their role in disease have been extensively studied during the last decade [22, 23], the interactions within mixed biofilms consisting of bacteria and fungi including Candida spp. have not been studied in depth. Furthermore, the majority of the previous studies on interactions between Candida and bacteria in mixed biofilms have focused on C. albicans and there are only a few studies on non-albicans Candida spp.