This section last updated: 2021-06-05 (2 years ago)
Author: David Baorto, MD, PhD
Date Written: 2011-05-12
There is a phenomenon by which the organism can appear to be susceptible to lincosamindes such as clindamycin when tested in vitro, yet exposure to an appropriate macrolide (such as erythromycin) can INDUCE resistance to the clindamycin. This mechanism of resistance involves methylation of the 23S rRNA binding site that is shared by 3 antibiotic classes (macrolides, lincosamides, and group B streptogramins) and prevents their binding to the site and exerting their effect. This resistance mechanism is known (for short) as MLSB.
When one of the erm methylases is produced constitutively, the resistance is constitutive and requires no induction. However, in some cases, the translation of the erm methylase protein is suppressed and is activated only after the binding of a macrolide antibiotic to upstream sequences, which alters the mRNA conformation, allowing it to be translated. Once this occurs, active methylase enzyme is produced which methylates the binding site for all 3 antibiotic classes, potentially preventing the binding of any of these antibiotic classes and inducing co-resistance. Detection of this resistance pattern can be detected phenotypically using disc diffusion (Clindamycin.induced [Susceptibility] by Disk diffusion (KB), 42720-3).
The methylase enzyme is encoded by one of the erm genes, generally ermA or ermC in staph, ermB in strep. Finding ermA or ermC similarly indicates the possibility for resistance to both erythromycin and clindamycin in Staph (either constitutive or inducible for clinda), so reporting both genes has been combined in some assays to indicate that one of the two has been detected (Erythromyin+clindamycin resistance ermA + ermC genes [Presence] by Molecular method, 62258-9).