Volume 1 • Issue 1 • 1000e101 J Antimicro ISSN: 2472-1212 Antimicro, an open access journal Open Access Editorial Santos et al., J Antimicro 2015, 1:1 DOI: 10.4172/2472-1212.1000e101 Journal of Antimicrobial Agents J o u r n a l o f A n t i m i c r o b i a l A g e n t s ISSN: 2472-1212 Editorial Fungal diseases afect a considerable proportion of the worldwide population, ranging in severity from mild supericial infections to grave invasive diseases [1-7]. he emergence and spread of systemic life-threatening fungal infections have increased in the last three decades, causing a major and alarming global concern [1- 7]. he more widespread provision of new medical practices (e.g., immunosuppressive therapy, use of broad spectrum antibiotics and invasive surgical procedures such as solid organ and bone marrow transplantation) and the greater number of people sufering from predisposing conditions (e.g., immunocompromising status such as neutropenia, diabetes and human immunodeiciency virus infection, low-birth-weight newborns, burns, patients with cancer and critically ill patients requiring implanted medical devices or grats) are the main factors that have been implicated in the augmented number of fungal infections [8-12] (Figure 1). he high morbidity and mortality associated with fungal infections is compounded by the limited therapeutic options and the emergence of drug-resistant fungi [13-17]. Timely and adequate interventions are necessary to maximize favorable outcomes, culminating in a successful treatment. Improved antifungal strategies are therefore urgently required [13-17]. In this context, the anti-virulence strategy is in vogue and is a light at the end of the tunnel considering the limited antifungal armamentarium [18-20]. In theory, the anti-virulence therapy prevents the emergence of resistance against a particular drug, since it inhibits the expression of virulence attribute(s) that are essential for the development of infection, without inhibiting the microbial proliferation [18-20]. Fungi are able to produce an arsenal of virulence factors [21-24], including the ability to form bioilm in both biotic (e.g., host tissues such as the oral cavity, respiratory, gastrointestinal and urinary tracts) and abiotic surfaces (e.g., implanted medical devices such as venous catheters, cannulation, pacemakers, endotracheal tubes, ventriculoperitoneal shunts, prosthetic joints, breast implants, contact or intraocular lenses, stents, intrauterine contraceptive devices and dentures) [24-27]. Alarming statistics on this theme corroborate the relevance of bioilm-related diseases: (i) the National Institutes of Health (NIH, USA) estimated that microbial bioilms (including both bacterial and fungal bioilms) were responsible for over 80% of all infections in USA [28], (ii) approximately 500,000 intravascular device-related bloodstream infections occur in USA each year [29], (iii) the majority of bloodstream infections are caused by infected central venous catheters, which is correlated with prolongation of hospital stay and added costs to the health care system, resulting in an estimated cost of US$ 11 billion annually [30-32]. Bioilm is the predominant growth lifestyle of many microorganisms, including several human opportunistic fungal pathogens (e.g., Candida albicans, non-albicans Candida species, Cryptococcus neoformans, Cryptococcus gatti, Trichosporon asahii, Rhodotorula spp., Aspergillus fumigatus, Malassezia pachydermatis, Histoplasma capsulatum, Coccidioides immitis, Pneumocystis spp., Fusarium spp. and many others), and is deined as a community of microorganisms encapsulated in a self-produced extracellular polymeric substance (or extracellular matrix) attached to a surface [33-36]. he bioilm extracellular matrix is mainly composed by polysaccharides, proteins, lipids and DNA, which form a robust shelter that ofers a protected and nutritionally rich environment, contributing to survival, molecule exchanges and proliferation [37]. he analysis of the A. fumigatus bioilm extracellular matrix by solid-state nuclear magnetic resonance spectroscopy revealed approximately 43% polysaccharide, 40% protein, 14% lipid and 3% aromatic-containing components [38]. he formation of a microbial bioilm can be didactically summarized in ive sequential steps: (i) adherence of cells to a surface, (ii) initial formation of colonies, (iii) secretion of extracellular polymeric substances, (iv) maturation in a three-dimensional structure and (v) cell dispersion [39]. Taking into account the clinical perspective, bioilms are intrinsically resistant to (i) conventional antifungal drugs, (ii) host immune responses and (iii) several environmental stress conditions, *Corresponding author: André L.S. Santos, Laboratório de Investigação de Peptidases (LIP), Departamento de Microbiologia Geral, Instituto de Microbiologia Paulo de Góes (IMPG), Bloco E - subsolo, sala 05, Centro de Ciências da Saúde (CCS), Universidade Federal do Rio de Janeiro (UFRJ), Rio de Janeiro, RJ 21941- 902, Brazil, Tel: +55 21 3938 6740; E-mail: andre@micro.ufrj.br Received December 21, 2015; Accepted December 28, 2015; Published December 31, 2015 Citation: Santos ALS, Thaís P. Mello, Ramos LS, Branquinha MH (2015) Bioilm: A Robust and Eficient Barrier to Antifungal Chemotherapy. J Antimicro 1: e101. doi:10.4172/2472-1212.1000e101 Copyright: © 2015 Santos ALS, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. Biofilm: A Robust and Efficient Barrier to Antifungal Chemotherapy André LS Santos 1,2* , Thaís P. Mello 1 , Lívia S. Ramos 1 and Marta H. Branquinha 1 1 Laboratório de Investigação de Peptidases, Departamento de Microbiologia Geral, Instituto de Microbiologia Paulo de Góes, Brazil 2 Programa de Pós-Graduação em Bioquímica, Instituto de Química, Universidade Federal do Rio de Janeiro, Brazil Fungal virulence attributes Host immune status Hospital environment Figure 1: The fungal disease is the consequence of the direct interaction among fungi, host and environment. In this context, the ability of fungal cells to produce numerous () attributes of virulence during the infection of an immunosuppressed host (), for example, attended at a hospital setting (e.g., interned at intensive therapy unit) culminates in the establishment of successful fungal disease.