chapter  14
36 Pages

Candida Biofi lms and the Host: Models and New Concepts for Eradication

Biofilms, adherent microbial communities embedded in a polymer matrix, are common in nature. However, they are also a persistent cause of hygiene problems in the food industry and in the medical field [1]. Biofilms result from a natural tendency of microbes to attach to biotic or abiotic surfaces, which can vary from mineral surfaces and mammalian tissues to synthetic polymers and indwelling medical devices, and to further grow on these substrates [2-4]. Candidiasis, caused most frequently by Candida albicans, and to a lesser extent by C. glabrata, C. tropicalis, or C. parapsilosis, is often associated with the formation of biofilms on the surface of medical devices and tissues [5]. Candida albicans is a dimorphic fungus and is part of the commensal human micoflora. It is also an opportunistic pathogen of the human body when its proliferation is not controlled by the host immune system. It is one of the most often identified agents in

nosocomial infections and is capable of invading virtually any site of the human host, from deep tissues and organs, to superficial sites such as skin and nails, to medical implants and catheters [6]. C. albicans biofilm development has been characterized in various model systems both in vitro and in vivo [7-9] and consists of distinct phases. The initial step consists of the adhesion of fungal cells of the yeast form to the substrate. It is followed by a phase of cell filamentation and proliferation, which results in the formation of multiple layers of sessile cells of different morphologies, including pseudohyphal and hyphal cells. The next step of maturation results in a complex network of cells embedded in extracellular polymeric material, composed of carbohydrates, proteins, hexosamine, phosphorus and uronic acid, as well as host constituents in natural settings [10]. There is indeed evidence that host glycoproteins, nucleic acids, and cells, such as neutrophils, may participate in the maturity of the matrix, in particular on mucosal sites [11-13]. The establishment of the biofilm extracellular matrix (ECM) represents a unique characteristic of biofilms. Quantity and composition of the matrix vary from one species to another and in different sites of infection depending on environmental cues, such as nutrient availability and mechanical stimuli [14-17]. Matrix synthesis by Candida biofilm cells has been shown to be minimal in static conditions in comparison to dynamic environments [10], aggravating biofilm formation on mucosal and abiotic sites where there is a fluid flow, such as on the oral mucosa, the urethra, or central venous catheters. The last step, dispersion of cells from a biofilm, plays a key part in the biofilm developmental cycle as it is associated with candidemia and disseminated invasive disease [18].