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“Background Linezolid is considered to as the last treatment option for infections caused by methicillin-resistant Staphylococcus

aureus (MRSA), vancomycin-resistant Enterococci and penicillin-resistant Streptococcus[1]. Mutations in the drug target site (23S rRNA or ribosomal proteins L3 and L4) are the most common mechanisms of linezolid resistance. Due to the low frequency of target mutation, the frequency of linezolid resistance is also relatively low [2]. However, emergence of the transferable linezolid resistance gene, cfr, in clinical isolates poses a challenge in linezolid treatment. cfr gene encodes an RNA methyltransferase, which modifies the adenine residue at position 2503 of the 23S rRNA gene and thereby confers resistance to phenicols, lincosamides, oxazolidinones, pleuromutilins, and streptogramin A antibiotics (the PhLOPSA phenotype) as well as decreases susceptibility to the 16-membered macrolides spiramycin and josamysin [3–5].