On fusidic acid resistance in Staphylococcus Aureus.

摘要: Controlling bacterial infections with antibiotics is central to modern health care. However, increasing resistance threatens effective therapy. This thesis concerns the use of antibiotic fusidic acid, and novel analogues treat topical caused by pathogen Staphylococcu aureus. It also addresses genetic mechanisms which S. aureus develops acid.Pre-clinical microbiological tests were made on two structurally different groups acid developed Leo Pharma. These drugs tested against Streptococcus pyogenes strains, measuring MIC, in vitro concentration-dependent bacteriocidal or bacteriostatic effects, vivo efficacy clearing infections. We a new superficial skin infection animal model (the ‘tape-stripping model’) designed for testing antibiotics, including analogues, pyogenes. Some compounds giving promising results will be further Fusidic inhibits protein synthesis binding elongation factor EF-G ribosome. Previously described are mutations gene coding (fusA), or, some presence (fusB, fusC fusD) that protects from acid.We discovered classes spontaneous FusR mutants small colony variant (SCV) phenotype associated persistent The SCV’s very frequent, slow growing, cross-resistant aminoglycosides, auxotrophic hemin menadione. SCV structural domain V (classic fusA map overwhelmingly III). remaining unmapped but their additive effect MIC together fusB plasmid suggests possibility mechanism translation machinery.