In vitro Comparison of Anti-Biofilm Effects against Carbapenem-Resistant Acinetobacter baumannii: Imipenem, Colistin, Tigecycline, Rifampicin and Combinations
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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. baumanniistrains with diverse resistance mechanisms (OXA-51, IMP-1 and VIM-2 type β-lactamases), and intended to compare the effectof each antibiotic regimen (rifampicin, colistin, imipenem, tigecycline, rifampicin-imipenem and rifampicin-colistin) on matureA. 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 (opticaldensity, 8.04 ± 2.16 vs. 0.49 ± 0.26). Regarding VIM-2 strains, none of imipenem, colistin and rifampicin reduced biofilm formationalone 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 synthesiscompared to the positive controls at 48 hours after incubation (P<0.01). Tigecycline inhibited biofilm formation even atthe one fourth level of MIC (1.17 ± 0.21). Likewise, both imipenem and colistin were also effective even with the reduced concentrationswhen those were combined with rifampicin. Such biofilm-inhibiting effects with those antibiotic regimens sustainedup to 96 hours after incubation. Conclusion: Tigecycline, imipenem-rifampicin and colistin-rifampicin would be effective for the prevention or reduction of biofilmformation caused by A. baumannii strains.
Abstract
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. baumanniistrains with diverse resistance mechanisms (OXA-51, IMP-1 and VIM-2 type β-lactamases), and intended to compare the effectof each antibiotic regimen (rifampicin, colistin, imipenem, tigecycline, rifampicin-imipenem and rifampicin-colistin) on matureA. 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 (opticaldensity, 8.04 ± 2.16 vs. 0.49 ± 0.26). Regarding VIM-2 strains, none of imipenem, colistin and rifampicin reduced biofilm formationalone 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 synthesiscompared to the positive controls at 48 hours after incubation (P<0.01). Tigecycline inhibited biofilm formation even atthe one fourth level of MIC (1.17 ± 0.21). Likewise, both imipenem and colistin were also effective even with the reduced concentrationswhen those were combined with rifampicin. Such biofilm-inhibiting effects with those antibiotic regimens sustainedup to 96 hours after incubation. Conclusion: Tigecycline, imipenem-rifampicin and colistin-rifampicin would be effective for the prevention or reduction of biofilmformation caused by A. baumannii strains.
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