The review was thought in the sad circumstance of the passing away of Bill, remembered as a charming Maestro for a large number of colleagues and students ( Ehrlich and Arciola, 2012). The profound influence that the Costerton's insight exerted on the bio-molecular knowledge of bacterial adhesion and on the need of appropriate medical methods for diagnosis and treatment of biofilm-related infections is analyzed in a review written by one of us together with the Director of the Costerton's Institute. The introduction of the biofilm theory opened two lines of research: the study of biochemistry and genetics of biofilms and their formation and, on the other side, the improvement of the medical diagnosis and treatment of biofilm-centered infections. Costerton's observations shifted the medical research from the attention to microbial cell-wall structures, which are the interface of planktonic bacteria with the environment, to the biofilm, which is the interface of sessile bacteria with their environment ( Costerton, 1989). The medical importance of bacterial biofilm was for the first time enlighten by Bill Costerton, recognized as the “Father of Biofilm,” who, in 1978 established an extraordinarily new microbiological paradigm, the “biofilm theory.” In an article, published in Scientific American, he asserted that bacteria stick on available surfaces in glycocalyx-enclosed biofilms and that the sessile bacterial population becomes predominant particularly in medical ecosystems ( Costerton et al., 1978). The description of specific extracellular polymeric components that structurally contribute to slime composition started with the second half of the century, when Wilkinson (1958) and Catlin and Cunningham (1958) began to report the existence of extracellular polysaccharides and deoxyribonucleic acids. Impressively, the first papers describing the ability of bacterial species to form slime date back to the beginning of the 20th century. The recognition of “slime” as a mucilaginous material elaborated by certain microrganisms such as molds and bacteria represents a very early discovery in the history of microbiology. aureus favors opsonophagocytosis and is a potential candidate for immune-protection.
In the search of vaccines against staphylococcal infections deacetylated PNAG retained on the surface of S. Interfering with the QS system is a much debated strategy to combat biofilm-related infections. A role is played by the quorum sensing system, which negatively regulates biofilm formation, favoring the dispersal phase that disseminates bacteria to new infection sites. aureus undergo to a phase variation for the biofilm production that has been ascribed, in turn, to the transposition of an insertion sequence in the icaC gene or to the expansion/contraction of a tandem repeat naturally harbored within icaC. epidermidis ica-independent alternative mechanisms of biofilm production have been described. The expression of ica locus is affected by environmental conditions. The product of icaB is an N-deacetylase responsible for the partial deacetylation of PIA. The product of icaC is involved in the externalization of the nascent polysaccharide. The product of icaD gives optimal efficiency to IcaA. The product of icaA is an N-acetylglucosaminyltransferase that synthetizes PIA oligomers from UDP- N-acetylglucosamine. lugdunensis, however, produces a biofilm prevalently consisting of proteins. DNA sequences homologous to ica locus are present in many coagulase-negative staphylococcal species, among which S. PIA is a poly-β(1-6)- N-acetylglucosamine (PNAG), partially deacetylated, positively charged, whose synthesis is mediated by the icaADBC locus. The extracellular polymeric substances of staphylococcal biofilms are the polysaccharide intercellular adhesin (PIA), extracellular-DNA, proteins, and amyloid fibrils. Biofilm formation is the main pathogenetic mechanism leading to the chronicity and irreducibility of infections.
Staphylococcus aureus and Staphylococcus epidermidis are the leading etiologic agents of implant-related infections. 2Department of Experimental, Diagnostic and Specialty Medicine (DIMES), University of Bologna, Bologna, Italy.1Research Unit on Implant Infections, Rizzoli Orthopaedic Institute, Bologna, Italy.
Carla Renata Arciola 1,2 *, Davide Campoccia 1, Stefano Ravaioli 1,2 and Lucio Montanaro 1,2
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