Advances in Vancomycin Resistance: Research inStaphylococcus aureus

Le résumé fourni par la source

This chapter concentrates on the mechanisms and biological features of vancomycin resistance in methicillin- and cephem-resistant Staphylococcus aureus (MRSA). Vancomycin-resistant S. aureus (VRSA) strains isolated from three American patients contained plasmids carrying the vanA gene complex. The gene complex is carried on a transposon which seems to have been transferred by conjugation from vancomycin-resistant enterococcus (VRE) that coexisted in the patients' bodies. The enzyme encoded by the vanA gene, together with those encoded by the adjacent genes vanH, vanX, and vanY, replaces D-alanyl-D-alanine residues of S. aureus peptidoglycan by D-alanyl-D-lactate. In the cell wall of Mu50, peptidoglycan crosslinking is significantly decreased as compared to hetero-vancomycin-intermediate S. aureus (VISA) strain Mu3 or vancomycin susceptible S. aureus (VSSA) strains. That is, there are more D-alanyl-D-alanine false targets in the cell-wall peptidoglycan layers of Mu50 than in those of control strains. The vancomycin resistance of VISA is not due to the acquisition of a resistance gene from another bacterial species. It is generated spontaneously from VSSA strains in vitro, though the development of the VISA phenotype does not occur through a single-step selection process. A remarkable feature of hetero-VISA is that it can be obtained from the VSSA strain by selection with beta-lactam antibiotics. A high-thoroughput sequencing strategy for regulator genes in combination with microarray transcription profiling in many isogenic VISA and hetero-VISA combinations might reveal several alternative series of regulator mutations.

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