AI Article Synopsis
- - The study investigates the effectiveness of fosfomycin as a treatment against multi-resistant A. baumannii infections and aims to understand its resistance mechanisms by analyzing 32 bacterial isolates.
- - Results showed a wide range of fosfomycin susceptibility (MIC values from 32 to ≥256 mg/L), with specific resistance genes found in some isolates, including mutations in key metabolic pathways.
- - Key findings include the absence of fosA and fosB genes in all isolates, presence of the fosX gene in four, and notable mutations in the MurA enzyme and adenylate cyclase that may impact fosfomycin resistance mechanisms in A. baumannii.
Article Abstract
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.
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| http://dx.doi.org/10.1016/j.meegid.2021.104943 | DOI Listing |
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