Vancomycin resistance in Staphylococcus aureus may occur faster than expected

Staphylococcus aureus , one notable example of nosocomial infections, has the characteristic ability to acquire antimicrobial resistance. Methicillin-resistant S. aureus have already become endemic worldwide, and vancomycin is the terminal antibiotic of choice for treatment of infections by these strains. Because of selection of vancomycin as the treatment option, n ow, the emergence of vancomycin resistance in S. aureus has been increasing elsewhere. Further, there is no consensus definition of minimum inhibitory concentration to determine the levels of vancomycin resistance in these strains making it difficult in interpretation and management of the resistant strains. As an intervention against cell wall physiology of the bacteria, vancomycin binds with terminal dipeptide of the peptidoglycan monomer. However, vancomycin-resistant strains possess a thickened cell wall with many free monomers capable of binding with the drug. The thickened cell wall not only traps more vancomycin molecules on the immediate cell surface, but also significantly impedes action of the drug towards inner layers of the peptidoglycan network on bacteria. Thus, the normal inner layers of peptidoglycan ensure the structural integrity of cell as a whole. Compounding with the stress selection of vancomycin-resistance in S. aureus , the novel mechanism allows the bacteria to reduce susceptibility to the drug easily; hence, emergence of vancomycin resistant strains in the hospital environment may occur faster than expected. ？ DOI: 10.3126/ijls.v3i0.2302