In vivo emergence of colistin resistance in Acinetobacter baumannii clinical isolates of sequence type 357 during colistin treatment

Yoonjung Kim, Il Kwon Bae, Hyukmin Lee, Seokhoon Jeong, DongEun Yong, Kyungwon Lee

Research output: Contribution to journalArticle

26 Citations (Scopus)

Abstract

This study was performed to investigate the mechanisms of in vivo acquisition of colistin resistance in A. baumannii during colistin treatment. Three colistin-susceptible/resistant pairs of A. baumannii were recovered from patients who underwent colistin treatment. All of the 6 isolates included in this study shared an identical sequence type (ST), ST375, and they showed identical SmaI-macrorestriction patterns by pulsed-field gel electrophoresis. The individual colistin-resistant isolates harbored distinct mutations in the pmrB gene. Mutations detected in the pmrB gene were Ala227Val, Pro233Ser, and frame shift from Phe26. In matrix-assisted laser desorption ionization-time of flight analysis, colistin-resistant isolates were different from their colistin-susceptible counterparts, and they showed additional distinct peaks at 1852 m/z, 1937 m/z, 1954 m/z, 1975 m/z, 2034 m/z, and 2157 m/z. In vivo selection of colistin-resistant A. baumannii occurred independently in strains of ST357 during colistin treatment, and the strains acquired colistin resistance via mutations in the pmrB gene resulting in modification of lipid A components.

Original languageEnglish
Pages (from-to)362-366
Number of pages5
JournalDiagnostic Microbiology and Infectious Disease
Volume79
Issue number3
DOIs
Publication statusPublished - 2014 Jan 1

Fingerprint

Colistin
Acinetobacter baumannii
Therapeutics
Mutation
Genes
Lipid A
Pulsed Field Gel Electrophoresis
Lasers

All Science Journal Classification (ASJC) codes

  • Microbiology (medical)
  • Infectious Diseases
  • Medicine(all)

Cite this

@article{ff48f0fa38a34b80b5b6958791987ed8,
title = "In vivo emergence of colistin resistance in Acinetobacter baumannii clinical isolates of sequence type 357 during colistin treatment",
abstract = "This study was performed to investigate the mechanisms of in vivo acquisition of colistin resistance in A. baumannii during colistin treatment. Three colistin-susceptible/resistant pairs of A. baumannii were recovered from patients who underwent colistin treatment. All of the 6 isolates included in this study shared an identical sequence type (ST), ST375, and they showed identical SmaI-macrorestriction patterns by pulsed-field gel electrophoresis. The individual colistin-resistant isolates harbored distinct mutations in the pmrB gene. Mutations detected in the pmrB gene were Ala227Val, Pro233Ser, and frame shift from Phe26. In matrix-assisted laser desorption ionization-time of flight analysis, colistin-resistant isolates were different from their colistin-susceptible counterparts, and they showed additional distinct peaks at 1852 m/z, 1937 m/z, 1954 m/z, 1975 m/z, 2034 m/z, and 2157 m/z. In vivo selection of colistin-resistant A. baumannii occurred independently in strains of ST357 during colistin treatment, and the strains acquired colistin resistance via mutations in the pmrB gene resulting in modification of lipid A components.",
author = "Yoonjung Kim and Bae, {Il Kwon} and Hyukmin Lee and Seokhoon Jeong and DongEun Yong and Kyungwon Lee",
year = "2014",
month = "1",
day = "1",
doi = "10.1016/j.diagmicrobio.2014.03.027",
language = "English",
volume = "79",
pages = "362--366",
journal = "Diagnostic Microbiology and Infectious Disease",
issn = "0732-8893",
publisher = "Elsevier Inc.",
number = "3",

}

TY - JOUR

T1 - In vivo emergence of colistin resistance in Acinetobacter baumannii clinical isolates of sequence type 357 during colistin treatment

AU - Kim, Yoonjung

AU - Bae, Il Kwon

AU - Lee, Hyukmin

AU - Jeong, Seokhoon

AU - Yong, DongEun

AU - Lee, Kyungwon

PY - 2014/1/1

Y1 - 2014/1/1

N2 - This study was performed to investigate the mechanisms of in vivo acquisition of colistin resistance in A. baumannii during colistin treatment. Three colistin-susceptible/resistant pairs of A. baumannii were recovered from patients who underwent colistin treatment. All of the 6 isolates included in this study shared an identical sequence type (ST), ST375, and they showed identical SmaI-macrorestriction patterns by pulsed-field gel electrophoresis. The individual colistin-resistant isolates harbored distinct mutations in the pmrB gene. Mutations detected in the pmrB gene were Ala227Val, Pro233Ser, and frame shift from Phe26. In matrix-assisted laser desorption ionization-time of flight analysis, colistin-resistant isolates were different from their colistin-susceptible counterparts, and they showed additional distinct peaks at 1852 m/z, 1937 m/z, 1954 m/z, 1975 m/z, 2034 m/z, and 2157 m/z. In vivo selection of colistin-resistant A. baumannii occurred independently in strains of ST357 during colistin treatment, and the strains acquired colistin resistance via mutations in the pmrB gene resulting in modification of lipid A components.

AB - This study was performed to investigate the mechanisms of in vivo acquisition of colistin resistance in A. baumannii during colistin treatment. Three colistin-susceptible/resistant pairs of A. baumannii were recovered from patients who underwent colistin treatment. All of the 6 isolates included in this study shared an identical sequence type (ST), ST375, and they showed identical SmaI-macrorestriction patterns by pulsed-field gel electrophoresis. The individual colistin-resistant isolates harbored distinct mutations in the pmrB gene. Mutations detected in the pmrB gene were Ala227Val, Pro233Ser, and frame shift from Phe26. In matrix-assisted laser desorption ionization-time of flight analysis, colistin-resistant isolates were different from their colistin-susceptible counterparts, and they showed additional distinct peaks at 1852 m/z, 1937 m/z, 1954 m/z, 1975 m/z, 2034 m/z, and 2157 m/z. In vivo selection of colistin-resistant A. baumannii occurred independently in strains of ST357 during colistin treatment, and the strains acquired colistin resistance via mutations in the pmrB gene resulting in modification of lipid A components.

UR - http://www.scopus.com/inward/record.url?scp=84902073922&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=84902073922&partnerID=8YFLogxK

U2 - 10.1016/j.diagmicrobio.2014.03.027

DO - 10.1016/j.diagmicrobio.2014.03.027

M3 - Article

C2 - 24809861

AN - SCOPUS:84902073922

VL - 79

SP - 362

EP - 366

JO - Diagnostic Microbiology and Infectious Disease

JF - Diagnostic Microbiology and Infectious Disease

SN - 0732-8893

IS - 3

ER -