Affiliation:
1. Department of Bacteriology
2. Department of Infection Control Science, Faculty of Medicine, Juntendo University, 2-1-1 Bunkyo-Ku, Tokyo, Japan 113-8421
Abstract
ABSTRACT
Multistep genetic alteration is required for methicillin-resistant
Staphylococcus aureus
(MRSA) to achieve the level of vancomycin resistance of vancomycin-intermediate
S. aureus
(VISA). In the progression of vancomycin resistance, strains with heterogeneous vancomycin resistance, designated hetero-VISA, are observed. In studying the whole-genome sequencing of the representative hetero-VISA strain Mu3 and comparing it with that of closely related MRSA strains Mu50 (VISA) and N315 (vancomycin-susceptible
S. aureus
[VSSA]), we identified a mutation in the response regulator of the
graSR
two-component regulatory system. Introduction of mutated
graR
, designated
graR
*, but not intact
graR
, designated
graRn
, could convert the hetero-VISA phenotype of Mu3 into a VISA phenotype which was comparable to that of Mu50. The same procedure did not appreciably increase the vancomycin resistance of VSSA strain N315, indicating that
graR
* expression was effective only in the physiological milieu of hetero-VISA cell to achieve a VISA phenotype. Interestingly, the overexpression of
graR
* increased the daptomycin MICs in both Mu3 and N315 and decreased the oxacillin MIC in N315.
Publisher
American Society for Microbiology
Subject
Infectious Diseases,Pharmacology (medical),Pharmacology
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