Acinetobacterhas emerged as one of the most important nosocomial microorganisms. Of particular concern is the extremely-multidrug-resistantAcinetobacter baumannii(A. baumannii), resistant to almost all available antibiotics and associated with high mortality rates. Colistin is often the only remaining treatment. Nevertheless, colistin-resistant and heteroresistant, defined as a colistin-susceptible isolate with subpopulation growing at >2 mg/L colistin, clinical isolates have been reported.
The aim of this study was to compare colistin MIC methodologies, determine heteroresistance, clonality and correlate them to patient outcome.
We used 172 A. baumanniiisolates that were collected in Tel Aviv Sourasky Medical Center (TASMC) between July 2006 and June 2011: 83 and 89 isolates from patients who died ≤14 days of bacteremia onset (defined as cases) and from patients who survived >14 days (defined as controls ) respectively. Typing of the bacterial isolates was performed by sequence-typing of theblaOXA-51 geneand REP-PCR. For 31 isolates, colistin MIC, using VITEK, agar dilution, microdilution and E-test, and heteroresistance were determined.
We found that 124 of the bacterial isolates (72%) had the OXA-66 gene. REP-PCR further divided this group into two major clones, REP1 and REP2. The lowest mortality was in group OXA-66 REP1 (16.66%), with highest mortality in OXA-66 REP2 (65.7%) and OXA-71 (63.6%). Colistin MICs, as determined by agar dilution and microdilution, were 0.25-1 mg/L. Similarly, MICs <0.5 mg/L were obtained using the E-test and VITEK. 87% of the thirty one tested isolates showed colistin heteroresistance. Overall the present work stresses the need to evaluate the clinical significance of thesein vitroobservations to colistin treatment failure. In addition, the promising correlation between the typing and patient outcome should be farther examined.
