I would like to compare my experience with the isolation of coagulase-negative staphylococci after linezolid therapy, and consequent linezolid-resistance based on several mutations occurring in domain V region and/or L3-L4-L22 proteins.
Very interesting observation. In my experience most mechanisms of microbial drug resistance are generally multifactorial in nature. There is an article that you might find interesting if you haven't read it already reporting similar findings in an ATCC strain of S. aureus. I have attached the article to this message.
Thank you very much for paper you suggested . I know this work and I followed quite the same way (but more complete) in the characterization of linezolid resistance in clinical CoNS strains that have developed resistance during therapy. It seems to demonstrate that linezolid is a mutagenic agent in always the same areas of ribosome. It's is quite similar to fluorquinolones against DNA-gyrase II and IV.
I couldn't agree more. There is also some speculation that oxygen radical generation may happen with many antibiotics independent of class which could explain these mutagenic effects, though I'm not certain of any specific studies with linezolid. I am more familiar with fluoroquinolone selected mutations in MRSA than in CoNS although there is likely overlap. Most of my work uses gene knockout and cloning in order to get some idea of resistance mechanisms. Are you taking a similar approach to that taken in this paper?
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