There is growing concern that vancomycin has diminished activity for methicillin-resistant Staphylococcus aureus ( Despite its sustained in vitro microbiologic inhibitory activity, clinicians now question the continued utility of vancomycin for methicillin-resistant Staphylococcus aureus (MRSA) infections (18,23). Within the past 5 years, multiple reports have described MRSA strains with vancomycin MICs at the high end of the CLSI susceptibility range (MICs of 2 mg/liter) (6,18,22). Data suggest that vancomycin has reduced activity against MRSA infections, with vancomycin MICs at the high end of the CLSI susceptibility range (6,11,16,19,20).At the Albany Medical Center Hospital (AMCH), a large proportion of the MRSA bloodstream isolates have vancomycin MICs at the high end of the CLSI susceptibility range. The MIC 50 and MIC 90 for the 76 MRSA bloodstream isolates (59 patients) obtained by using the Etest method and recovered between
These data indicate that, besides patient risk factors and third-generation cephalosporins, other antibiotics may provide selective pressures in maintaining ESBL organisms due to multiple resistance genes on plasmids. beta-Lactamase inhibitor combinations appear to be an acceptable substitute to third-generation cephalosporins in strategies to control ESBL organisms.
A patient's cumulative antibiotic exposure history is likely to be more important than any one specific exposure when determining the likelihood of developing a CIRE infection.
To study the effect of fluoroquinolone exposure on the expression of mec(A)-encoded oxacillin resistance, population analysis profiling was performed on four strains of fluoroquinolone-susceptible, mec(A)-positive, heteroresistant Staphylococcus aureus. Growth in the presence of 0.5 x MIC of a fluoroquinolone resulted in >10-fold increase in the proportion of the population that grew on agar containing oxacillin 128 mg/L. Ciprofloxacin exhibited a greater effect than moxifloxacin, levofloxacin and gatifloxacin (average 3400-, 220-, 170- and 49-fold increase in oxacillin-resistant colonies versus the control, respectively). The increase was directly proportional to the fluoroquinolone concentration and could be detected as early as 8 h after exposure to the fluoroquinolone. At 8 h, the absolute number of colonies that grew on oxacillin 128 mg/L was similar whether or not the isolate was exposed to the fluoroquinolone, but the total cfu on non-selective media decreased. The resultant oxacillin-resistant colonies also showed a 1.5- to 3-fold increase in fluoroquinolone MIC. No oxacillin resistance was observed on two similarly treated fluoroquinolone-susceptible, mec(A)-negative strains. It appears that fluoroquinolones influence oxacillin resistance by selective inhibition or killing of the more susceptible subpopulations in heteroresistant S. aureus. The surviving populations are more resistant to both oxacillin and fluoroquinolone. The mechanisms of resistance to the two agents may be unrelated but tend to be associated. This could explain in part the observed increases in fluoroquinolone-resistant MRSA.
Patients with MRSA bloodstream infections in the ICU or with a history of vancomycin exposure should be considered at high risk of infection with strains for which vancomycin MICs are elevated. Appropriate and aggressive empirical therapy is required for these patients.
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