This study examined the adherence of Neisseria meningitidis to human buccal epithelial cells (BEC). Past studies have utilized microscopic assays which are tedious and are, at high bacterial concentrations, relatively inaccurate. This study developed a rapid radioactive assay for bacterial adherence which gave results comparable to the microscopic assay. This new assay system was used, then, to examine the kinetics and specificity of meningococcal adherence. Adherence, which increased linearly as a function of multiplicity of infection, reached maximal values within 5 minutes. Adherence was mediated by a bacterial surface protein; pronase-treated meningococcidid not adhere well to BEC. Unlike other adherent Neisseria, adherent meningococci did not exhibit pill. Removal of the capsule with saccharolytic agents greatly increased adherence. These results suggest that Neisseria meningitidis may adhere to human BEC via a non-pilus surface protein which is partially masked by the capsule. The BEC receptor for this protein was examined but remains unidentified.

This thesis reports work carried out to investigate the adhesive properties of chlorinated-rubber based lacquers on mild steel. Tensile tests were used to measure the failure stresses of such coatings, and it was established that a mixture of cohesive and weak boundary layer failure occurred. Consideration was given to the influence of lacquer storage, film thickness, drying time and binder molecular weight on the failure stress of the coating. In Chapters 1 and 2 the theories of adhesion are discussed, the system under investigation is described and methods of testing the adhesive and cohesive strengths of coating/substrate systems are considered. The development of a suitable test method, preparation and testing of specimens are described in Chapter 3, and the experimental values of stress to cause failure of the coating are discussed. Chapter 4 describes the detailed surface analytical work which was carried out to establish the mode of failure of the coating, and investigate the inhomogeneities occurring within the cured film. It was found that the plasticiser migrated towards the lacquer/air interface as the film cured, leaving a "binder-rich" region at the lacquer/substrate interface. It was also found that chemical interaction occurred between the lacquer and the substrate, under certain circumstances, and in Chapter 5 these interactions are considered. Theoretical work was carried out to investigate the application of various expressions for calculating the Van der Waals forces acting between two molecules, to the system under investigation. This is described in Chapter 6. The numerical values of the Van der Waals forces obtained using these expressions are compared, and their relevance to the experimentally measured failure stresses considered. The conclusions which may be drawn from the results of the work described in Chapters 3-6 are considered in Chapter 7, and suggestions made of areas for further work.

No description available.

No description available.

No description available.

Serratia marcescens is an opportunistic pathogen involved in predominantly nosocomial infections, however, it is also implicated as a common cause of microbial keratitis. Since many S. marcecens strains are also resistant to multiple antibiotics, this organism represents a growing public health problem. S. marcescens MG1 utilises a regulatory system for regulation of swarming motility and exo-enzyme secretion that relies on the production of a diffusible signal identified as N-butanoyl-L-homoserine lactone (C4-HSL). The aim of this study was to determine the role of C4-HSL in surface colonisation (adhesion and biofilm formation). In this thesis, the development of a novel biofilm in S. marcescens MG1 is described. The biofilm comprises of an intricate and complex structure consisting of long filamentous cells, cell aggregates and cell chains. Two C4-HSL controlled genes (bsmA and bsmB) are shown to be crucial for biofilm formation. It is proposed that C4-HSL regulated bsmA and bsmB gene products are engaged in fine tuning aggregation at a specific time point in late biofilm development. Since adhesion is the first stage of colonisation, the role of C4-HSL in adhesion to a hydrophilic abiotic surface (HAS) and a human corneal epithelial (HCE) cell line was assessed. While adhesion to the HAS was found to be C4-HSL controlled, this was not the case for adhesion to the HCE cells. In adhesion to the HAS, mutations in the following C4-HSL regulated genes resulted in reduced adhesion; a sensor kinase gene (rssA), a type I transporter gene (lipB), bsmA and bsmB. These four genes were found to effect the expression of type I fimbriae which is proposed to be the adhesin affecting C4-HSL regulated adhesion. While C4-HSL is not involved in adhesion to the HCE cell line, the genes bsmA and bsmB are important. It is proposed that bsmA and bsmB dependent HCE adhesion is due to the requirement of these genes for type I fimbriae production. Furthermore, C4-HSL was found to regulate capsule polysaccharide and OmpX production and repress cytotoxic activity against HCE cells and erythrocytes. It is proposed that cytotoxicity is mediated by ShlA haemolysin.

Serratia marcescens is an opportunistic pathogen involved in predominantly nosocomial infections, however, it is also implicated as a common cause of microbial keratitis. Since many S. marcecens strains are also resistant to multiple antibiotics, this organism represents a growing public health problem. S. marcescens MG1 utilises a regulatory system for regulation of swarming motility and exo-enzyme secretion that relies on the production of a diffusible signal identified as N-butanoyl-L-homoserine lactone (C4-HSL). The aim of this study was to determine the role of C4-HSL in surface colonisation (adhesion and biofilm formation). In this thesis, the development of a novel biofilm in S. marcescens MG1 is described. The biofilm comprises of an intricate and complex structure consisting of long filamentous cells, cell aggregates and cell chains. Two C4-HSL controlled genes (bsmA and bsmB) are shown to be crucial for biofilm formation. It is proposed that C4-HSL regulated bsmA and bsmB gene products are engaged in fine tuning aggregation at a specific time point in late biofilm development. Since adhesion is the first stage of colonisation, the role of C4-HSL in adhesion to a hydrophilic abiotic surface (HAS) and a human corneal epithelial (HCE) cell line was assessed. While adhesion to the HAS was found to be C4-HSL controlled, this was not the case for adhesion to the HCE cells. In adhesion to the HAS, mutations in the following C4-HSL regulated genes resulted in reduced adhesion; a sensor kinase gene (rssA), a type I transporter gene (lipB), bsmA and bsmB. These four genes were found to effect the expression of type I fimbriae which is proposed to be the adhesin affecting C4-HSL regulated adhesion. While C4-HSL is not involved in adhesion to the HCE cell line, the genes bsmA and bsmB are important. It is proposed that bsmA and bsmB dependent HCE adhesion is due to the requirement of these genes for type I fimbriae production. Furthermore, C4-HSL was found to regulate capsule polysaccharide and OmpX production and repress cytotoxic activity against HCE cells and erythrocytes. It is proposed that cytotoxicity is mediated by ShlA haemolysin.

Thesis (Ph.D.)--McMaster University, 2005. / Supervisor: Robert H. Pelton. Includes bibliographical references. Also available online.

Thesis (Ph.D.)--McMaster University, 2005. / Supervisor: Robert H. Pelton. Includes bibliographical references. Also available online.

Diss. (sammanfattning) Stockholm : Karolinska institutet, 2001. / Härtill 4 uppsatser.