Journal article

Emergence of High-Level Colistin Resistance in an Acinetobacter baumannii Clinical Isolate Mediated by Inactivation of the Global Regulator H-NS

Deanna Deveson Lucas, Bethany Crane, Amy Wright, Mei-Ling Han, Jennifer Moffatt, Dieter Bulach, Simon L Gladman, David Powell, Jesus Aranda, Torsten Seemann, Diana Machado, Teresa Pacheco, Teresa Marques, Miguel Viveiros, Roger Nation, Jian Li, Marina Harper, John D Boyce

Antimicrobial Agents and Chemotherapy | AMER SOC MICROBIOLOGY | Published : 2018

Abstract

Colistin is a crucial last-line drug used for the treatment of life-threatening infections caused by multidrug-resistant strains of the Gram-negative bacterium Acinetobacter baumannii However, colistin-resistant A. baumannii isolates can still be isolated following failed colistin therapy. Resistance is most often mediated by the addition of phosphoethanolamine (pEtN) to lipid A by PmrC, following missense mutations in the pmrCAB operon encoding PmrC and the two-component signal transduction system PmrA/PmrB. We recovered a pair of A. baumannii isolates from a single patient before (6009-1) and after (6009-2) failed colistin treatment. These strains displayed low and very high levels of coli..

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Grants

Awarded by Fundacao para a Ciencia e a Tecnologia, Portugal


Funding Acknowledgements

The work performed in the Boyce laboratory was partially funded by The National Health and Medical Research Council, Canberra, Australia. The work performed in Viveiros Laboratory (Lisbon, Portugal) was supported by the Fundacao para a Ciencia e a Tecnologia, Portugal, through grants UID/Multi/04413/2013 (M.V. and D.M.) and SFRH/BPD/100688/2014 (D.M.).