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BACKGROUND: 2297, isolated from a patient treated with tigecycline for pneumonia, developed tigecycline resistance, in contrast to carbapenem-resistant isolate 1215, which was collected four months prior to the 2297 isolate. Mechanisms underlying tigecycline resistance were elucidated for the clinical isolates. METHODS: were determined by reverse-transcription quantitative PCR. RESULTS: gene promoter replacement resulting in stronger activation of the gene. CONCLUSIONS: isolate developed tigecycline resistance during tigecycline treatment. It was related to the overexpression of the AcrAB resistance-nodulation-cell division efflux system due to promoter replacement.
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Yoon et al. (2019) studied this question.
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