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Treatment of infections caused by A. baumannii is becoming a challenge due to the ability to develop multidrug-resistance, virulence, and high mortality. We described the colistin resistance and virulence genes present in six A. baumannii clinical isolates using WGS, expression by qPCR , and virulence in the Galleria mellonella model. The colistin-resistant isolates were assigned as ST233 and the colistin-susceptible isolates as ST236 and ST407. The colistin-resistant isolates contained mutations within PmrA/PmrB, and the pmr A showed up‐regulation in all of them. Only one colistin-resistant isolate indicating virulence in G. mellonella. This particular isolate belonged to a different clone, and it was the only isolate that presented non‐synonymous mutations in pmr B. Colistinresistance in A. baumannii isolates seems to be caused by up‐regulation of pmrA gene. Only one isolate appeared to be virulent in the G. mellonella model. This finding indicating low virulence in isolates belonging to emerging clones circulating in our hospital. [ABSTRACT FROM AUTHOR]

The treatment of infections caused by A. baumannii is a challenge and fosfomycin has been used as a combination therapy. Moreover, data regarding the fosfomycin resistance mechanism is scarce. The goals of this study were to evaluate fosfomycin susceptibility in polyclonal multi-resistant A. baumannii isolates and characterize the fosfomycin resistance. We analyzed 32 A. baumannii isolates from a Brazilian bacterial collection, followed by their minimum inhibitory concentration (MIC), and whole-genome sequence to detect fosfomycin resistance genes. The isolates showed a fosfomycin MIC ranging from 32 to ≥256 mg/L. All isolates were negative for fosA and fosB genes, and four isolates carried the fosX gene. Two different metabolic pathways that form peptidoglycan precursors were identified. Mutations were observed in the adenylate cyclase gene. All A. baumannii isolates studied showed Val132Ala substitutions in MurA. The analysis showed different ways that may lead to the intrinsic fosfomycin-resistance of A. baumannii, such as alterations on the glycerol-3-phosphate transporter system caused by adenylate cyclase mutations; and a possible connection of cell wall recycling by different metabolic pathways. • This study characterizes the genetic basis of fosfomycin resistance mechanisms in polyclonal multi-resistant clinical Acinetobacter baumannii isolates. • The analysis showed different ways that lead to the intrinsic fosfomycin-resistance of A. baumannii as alterations on the GlpT and a possible connection of cell wall recycling by different metabolic pathways. [ABSTRACT FROM AUTHOR]