SULM – Schweizerische Union für Labormedizin | Union Suisse de Médecine de Laboratoire | Swiss Union of Laboratory Medicine

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B. Berger-Bächi

1Department of Medical Microbiology, University of Zürich

All antibiotics introduced into therapy have been followed sooner or later by the development and spread of resistant pathogens, which have a formidable ability to adapt to changing environmental conditions. They demonstrate fascinating versatility and sophistication in the development of resistance mechanisms, favoured by their large numbers and short generation time. A given population of a strain always contains a certain fraction of spontaneous mutants. Such mutants with a small advantage will be selected by antibiotics and become the origin for the stepwise development of clinical resistance. This type of resistance formation is ongoing: Examples are the emerging vancomycin intermediate resistance in Staphylococcus aureus, which is due to chromosomal mutations and the growing number of extended spectrum beta-lactamases in Gram-negative pathogens, which arise through the mutational evolution of existing resistance determinants. An even more efficient way for bacteria to survive antibiotic action is the acquisition and dissemination of preformed resistance determinants by horizontal gene transfer. The unlimited use of antibiotics has greatly increased the genetic pool of mobile resistance determinants.
Although antibiotic resistance can be traced down to three strategies, including the inactivation of the drug, prevention of the antibiotic from reaching its target, and modification of the target, this goal can be attained by completely different mechanisms and strategies. Production of beta-lactamases; decrease of the outer membrane permeability in Gram-negatives; upregulation of export; modification of the target, such as the formation of mosaic-penicillin-binding proteins (PBP) in pneumococci or the recruiting of a resistant foreign PBP, such as PBP2a in methicillin-resistant staphylococci; or even down regulation of the metabolism, as seen in small colony variants, are all different mechanisms to attain the same goal, namely beta-lactam resistance.

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