In vitro Comparison of Anti-Biofilm Effects against Carbapenem-Resistant Acinetobacter baumannii: Imipenem, Colistin, Tigecycline, Rifampicin and Combinations

BACKGROUND Multi-drug resistant (MDR) Acinetobacter baumannii has emerged as one of the most important nosocomial pathogens. In addition to the diverse resistance mechanisms, some A. baumannii strains are known to have biofilm-producing capacity, thereby decreasing antibiotic effectiveness. MATERIALS AND METHODS This study was designed to assess biofilm-producing capacity of three different MDR A. baumannii strains with diverse resistance mechanisms (OXA-51, IMP-1 and VIM-2 type β-lactamases), and intended to compare the effect of each antibiotic regimen (rifampicin, colistin, imipenem, tigecycline, rifampicin-imipenem and rifampicin-colistin) on mature A. baumannii biofilms using in vitro polystyrene plate biofilm assay. RESULTS Among three MDR A. baumannii strains, only VIM-2 strain produced strong biofilm compared to the controls (optical density, 8.04 ± 2.16 vs. 0.49 ± 0.26). Regarding VIM-2 strains, none of imipenem, colistin and rifampicin reduced biofilm formation alone at MIC of each antibiotic agent (inhibition of biofilm synthesis, less than 30%). In comparison, tigecyclin (0.76 ± 0.23), imipenem-rifampicin (1.07 ± 0.31) and colistin-rifampicin (1.47 ± 0.54) showed a significant inhibition of biofilm synthesis compared to the positive controls at 48 hours after incubation (P<0.01). Tigecycline inhibited biofilm formation even at the one fourth level of MIC (1.17 ± 0.21). Likewise, both imipenem and colistin were also effective even with the reduced concentrations when those were combined with rifampicin. Such biofilm-inhibiting effects with those antibiotic regimens sustained up to 96 hours after incubation. CONCLUSION Tigecycline, imipenem-rifampicin and colistin-rifampicin would be effective for the prevention or reduction of biofilm formation caused by A. baumannii strains.