Antimicrobial Resistance Mechanisms and Virulence of Colistin- and Carbapenem-Resistant Acinetobacter baumannii Isolated from a Teaching Hospital in Taiwan

Acinetobacter baumannii, a Gram-negative bacterium, is an important nosocomial pathogen. Colistin-resistant A. baumannii is becoming a new concern, since colistin is one of the last-line antibiotics for infections by carbapenem-resistant A. baumannii. From 452 carbapenem-resistant isolates collected in a teaching hospital in Taipei, Taiwan, we identified seven that were resistant to colistin. Carbapenem resistance in these isolates is attributed to the presence of carbapenemase gene bla(OXA-23) in their genomes. Colistin resistance is presumably conferred by mutations in the sensor kinase domain of PmrB found in these isolates, which are known to result in modification of colistin target lipid A via the PmrB-PmrA-PmrC signal transduction pathway. Overexpression of pmrC, eptA, and naxD was observed in all seven isolates. Colistin resistance mediated by pmrB mutations has never been reported in Taiwan. One of the seven isolates contained three mutations in lpxD and exhibited an altered lipopolysaccharide profile, which may contribute to its colistin resistance. No significant difference in growth rates was observed between the isolates and the reference strain, suggesting no fitness cost of colistin resistance. Biofilm formation abilities of the isolates were lower than that of the reference. Interestingly, one of the isolates was heteroresistant to colistin. Four of the isolates were significantly more virulent to wax moth larvae than the reference.

Automated summary

In a teaching hospital in Taipei, Taiwan, seven carbapenem-resistant Acinetobacter baumannii isolates with colistin resistance were identified. The resistance to carbapenem was attributed to the bla(OXA-23) gene, while colistin resistance was likely due to mutations in the sensor kinase domain of PmrB. Overexpression of pmrC, eptA, and naxD genes were observed in all isolates, and some isolates with mutations in lpxD exhibited altered lipopolysaccharide profiles contributing to colistin resistance. No fitness cost was observed in the resistant isolates compared to the reference strain. Interestingly, one isolate showed heteroresistance to colistin, and four isolates were more virulent to wax moth larvae.