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Well, the simple answer to your question is no because the possible aminoglycoside-modifying enzymes that can be acquired by gram-positive organisms including MRSA have different substrate activities. For example, AAC(6)-APH(2) can inactivate both gentamicin, tobramycin, and amikacin. AAC(2-I) would inactivate gentamicin and tobramycin but not amikacin while APH(3)-III would inactivate amikacin but not gentamicin or tobramycin. Based on this alone, one could not predict amikacin resistance/susceptibility in MRSA based on the result of one or the other. Secondly, if you look at the suggested groupings of antimicrobial agents for testing against staphylococci in the most recent CLSI M100-S16 guidelines, you will notice that testing aminoglycosides falls under Group C (way down the list) and only Gentamicin is listed even though breakpoints exist for other aminoglycosides. This means that the amount of data accumulated for MRSA and amikacin is scant. A quick search in the TSN database indicates that fewer than 300 strains of S. aureus were tested nationally against amikacin and approximately 75% were susceptible and those couldn't be divided into MRSA and MSSA. Thirdly, if you search the literature for vancomycin/amikacin synergy versus MRSA you will find very little in terms of human outcomes results. In fact, the only study I could find was in a rabbit model of meningitis and only vancomycin and rifampin were found to be synergistic. Finally, there are very few studies documenting a correlation between in vitro synergy testing and outcome. For example, a study by Aaron and colleages (Lancet 2005, 366:463) demonstrated that treatment of cystic fibrosis patients based on in vitro synergy testing did not improve outcome any better than treatment based on single drug susceptibility testing. Different system, but many cf patients are colonized with MRSA. This is a pretty long winded way of saying "I don't think so" but there are very little data available to indicate otherwise.
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