Methicillin‐resistant Staphylococcus aureusにおけるarbekacinの高度耐性化について

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  • High resistance mechanisms of methicillin-resistant Staphylococcus aureus to arbekacin.

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Arbekacin (ABK)-highly resistant mutants were isolated from methicillin-resistant Staphylococcus aureus (MRSA) of clinical isolates which showed low resistance (1.56μg/ml of MIC) or sensitivity (0.78μg/ml of MIC) to ABK. The mutants derived from gentamicin (GM)(25μg/ml to 100μg/ml of MIC) and tobramycin (TOB) resistant strains expressed ABK resistance at a level of 12.5μg/ml or 25μg/ml of MIC, and at highly GM resistant levels equal to or exceeding 200μg/ml. Plasmid pMS 91 is a laboratory plasmid and confers GM (100μg/ml of MIC) and TOB (800μg/ml of MIC) resistances but is sensitive to ABK (0.78μg/ml of MIC) in S. aureus, and encodes a determinant for bifunctional aminoglycoside modifying enzymes of 6'-aminoglycosides acetyltransferase (AAC (6')) and 2''-aminoglycosides phosphotransferase (APH (2'')). ABK resistant mutants were isolated from S. aureus MS353 carrying pMS91, and the mutants expressed ABK and GM resistances at a level of 25μg/ml, and at levels equal to or exceeding 200μg/ml of MIC, respectively. The amount of the aminoglycoside modifying enzyme AAC (6')/APH (2'') in the mutant strain was six times more than that of the parent strain. The relative enzyme activities to ABK of the parent and mutant strains were 2% that of kanamycin (KM). These results indicate that the ABK-highly resistant mutant of GM-TOB resistant S. aureus resulted from an increased amount of the aminoglycoside modifying enzyme of AAC (6')/APH (2'').

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