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mlsb resistance may be constitutive or inducible.
mlsb resistens kan være konstitutiv eller induktiv.

resistant to erythromycin a by a constitutive mlsb mechanism.
er resistente overfor erythromycina ved en konstitutiv mlsb mekanisme.

telithromycin does not induce mlsb resistance in vitro to staphylococcus aureus, streptococcus b
telithromycin inducerer ikke in vitro mlsb resistens over for staphylococcus aureus, streptococcus pneumoniae og streptococcus pyogenes, en egenskab der tilskrives 3 ketonfunktionen.

this is often referred to as mlsb resistance as it affects macrolides, lincosamides and streptogramins.
der refereres ofte til dette som mlsb-resistens, da det har betydning for makrolider, lincosamider og streptograminer.

against erythromycin a resistant strains, due to an mlsb mechanism of resistance, telithromycin shows a more than 20 fold affinity b
over for erythromycin a resistente stammer udviser telithromycin på grund af en mlsb resistensmekanisme i den bakterielle b

strains, due to an mlsb mechanism of resistance, telithromycin shows a more than 20 fold affinity compared to erythromycin a in the 50s bacterial subunit.
resistente stammer udviser telithromycin på grund af en mlsb resistensmekanisme i den bakterielle 50s subunit en 20 gange så høj affinitet sammenlignet med erythromycin a. te

against erythromycin a resistant strains, due to an mlsb mechanism of resistance, telithromycin shows a more than 20 fold affinity compared to erythromycin a in the 50s bacterial subunit.
over for erythromycin a resistente stammer udviser telithromycin på grund af en mlsb resistensmekanisme i den bakterielle 50s subunit en 20 gange så høj affinitet sammenlignet med erythromycin a.

+ telithromycin is not active against organisms that constitutively express the mlsb resistance determinant (cmlsb).
+**telithromycin er ikke aktivt mod organismer, der grundlæggende udtrykker mlsb- resistensdeterminanten (cmlsb).

resistance to macrolides can develop by mutations in genes encoding ribosomal rna (rrna) or some ribosomal proteins; by enzymatic modification (methylation) of the 23s rrna target site, generally giving rise to cross-resistance with lincosamides and group b streptogramins (mlsb resistance); by enzymatic inactivation; or by macrolide efflux.
resistens mod macrolider kan udvikles ved mutation i gener der koder for ribosomal rna (rrna) eller nogle ribosomal proteiner; ved enzymatisk modifikation (metylering) af det specifikke 23s rrna, hvilket ofte giver krydsresistens med lincosamider og gruppe b-streptogramin (mlsb resistens); ved enzymatisk inaktivering eller ved macrolid efflux.