Absence of Alleviates Negative Growth Effects of Colistin Resistance in .

Jessie E Wozniak, Aroon T Chande, Eileen M Burd, Victor I Band, Sarah W Satola, Monica M Farley, Jesse T Jacob, I King Jordan, David S Weiss
Author Information
  1. Jessie E Wozniak: Emory Vaccine Center, Atlanta, GA 30317, USA.
  2. Aroon T Chande: Institute for Bioengineering and Biosciences, Georgia Institute of Technology, Atlanta, GA 30332, USA. ORCID
  3. Eileen M Burd: School of Medicine, Emory University, Atlanta, GA 30322, USA. ORCID
  4. Victor I Band: Emory Vaccine Center, Atlanta, GA 30317, USA.
  5. Sarah W Satola: School of Medicine, Emory University, Atlanta, GA 30322, USA.
  6. Monica M Farley: School of Medicine, Emory University, Atlanta, GA 30322, USA.
  7. Jesse T Jacob: School of Medicine, Emory University, Atlanta, GA 30322, USA. ORCID
  8. I King Jordan: School of Biological Sciences, Georgia Institute of Technology, Atlanta, GA 30332, USA.
  9. David S Weiss: Emory Vaccine Center, Atlanta, GA 30317, USA.

Abstract

Colistin is an important last-line antibiotic to treat highly resistant infections. Resistance to colistin has emerged among clinical isolates but has been associated with a significant growth defect. Here, we describe a clinical isolate with a deletion of , a regulator of colistin resistance, leading to high-level resistance in the absence of a growth defect. The identification of a path to resistance unrestrained by growth defects suggests colistin resistance could become more common in .

Keywords

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Grants

  1. P51 OD011132/NIH HHS
  2. R01 AI141883/NIAID NIH HHS
  3. David S. Weiss/Burroughs Wellcome Fund
  4. AI141883/NIH HHS

Word Cloud

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