Lazăr Veronica, Chifiriuc Mariana Carmen
University of Bucharest, Faculty of Biology, Dept. of Microbiology & Immunology, Romania.
Roum Arch Microbiol Immunol. 2010 Jul-Sep;69(3):125-38.
Recent public announcements stated that 60% to 85% of all microbial infections involve biofilms developed on natural tissues (skin, mucosa, endothelial epithelia, teeth, bones) or artificial devices (central venous, peritoneal and urinary catheters, dental materials, cardiac valves, intrauterine contraceptive devices, contact lenses, different types of implants). Prosthetic medical devices are risk factors of chronic infections in developed countries and these infections are characterized by slow onset, middle intensity symptoms, chronic evolution and resistance to antibiotic treatment. In case of biofilm development, a series of genes (40-60% of the prokaryotic genome) are modulated (activated/inhibited) by complex cell to cell signalling mechanisms and the biofilm cells become phenotypically distinct from their counterpart--free cells, being more resistant to stress conditions (including all types of antimicrobial substances); this resistance is phenotypical, behavioural and, more recently, called TOLERANCE. Four major mechanisms can account for biofilm antibiotic tolerance: (1) the failure of antibiotic penetration into the depth of a mature biofilm due to the biofilm matrix; (2) the accumulation of high levels of antibiotic degrading enzymes; (3) in the depth of biofilm, cells are experiencing nutrient limitation entering in a slow-growing or starved state; slow-growing or non-growing cells being not highly susceptible to antimicrobial agents, this phenomenon could be amplified by the presence of phenotypic variants or "persisters" and (4) biofilm's bacteria can turn on stress-response genes and switch to more tolerant phenotypes on exposure to environmental stresses; (5) genetic changes, probably selected by different stress conditions, such as mutations and gene transfer could occur inside the biofilm. In these conditions, biofilm associated infections require a different approach, both clinically and paraclinically.
最近的公开声明称，所有微生物感染中有60%至85%涉及在天然组织（皮肤、黏膜、内皮上皮、牙齿、骨骼）或人工装置（中心静脉导管、腹膜和导尿管、牙科材料、心脏瓣膜、宫内节育器、隐形眼镜、不同类型的植入物）上形成的生物膜。在发达国家，医用假体装置是慢性感染的危险因素，这些感染的特点是起病缓慢、症状中度、病程慢性且对抗生素治疗耐药。在生物膜形成的情况下，一系列基因（原核生物基因组的40%-60%）通过复杂的细胞间信号传导机制被调节（激活/抑制），生物膜细胞在表型上与其对应的游离细胞不同，对压力条件（包括所有类型的抗菌物质）更具抗性；这种抗性是表型的、行为的，最近被称为耐受性。生物膜抗生素耐受性可由四种主要机制解释：（1）由于生物膜基质，抗生素无法渗透到成熟生物膜的深部；（2）高水平抗生素降解酶的积累；（3）在生物膜深部，细胞因营养限制进入缓慢生长或饥饿状态；缓慢生长或不生长的细胞对抗菌剂不太敏感，这种现象可因表型变异体或“持留菌”的存在而放大；（4）生物膜中的细菌在暴露于环境压力时可开启应激反应基因并转换为更具耐受性的表型；（5）在生物膜内部可能发生遗传变化，可能是由不同的压力条件选择的，如突变和基因转移。在这些情况下，生物膜相关感染在临床和临床旁都需要不同的方法。
