TY - JOUR
T1 - Colistin-resistant acinetobacter baumannii
T2 - Beyond carbapenem resistance
AU - Qureshi, Zubair A.
AU - Hittle, Lauren E.
AU - O'Hara, Jessica A.
AU - Rivera, Jesabel I.
AU - Syed, Alveena
AU - Shields, Ryan K.
AU - Pasculle, Anthony W.
AU - Ernst, Robert K.
AU - Doi, Yohei
N1 - Funding Information:
Financial support. This work was supported by the National Institutes of Health (NIH) (grant numbers R01AI104895 to Y. D. and KL2TR000146 to R. K. S.). Y. D. was also supported by NIH (grant number R21AI107302).
Funding Information:
Potential conflicts of interest. R. K. S. has received research funding from Astellas Pharma and Merck & Co for studies unrelated to this work. R. K. E. has received research funding from MedImmune for a study unrelated to this work. Y. D. has served on an advisory board for Shionogi Inc, consulted for Melinta Therapeutics, and received research funding from Merck & Co for a study unrelated to this work. All other authors report no potential conflicts.
Publisher Copyright:
© 2015 The Author. Published by Oxford University Press on behalf of the Infectious Diseases Society of America. All rights reserved.
PY - 2015/5/1
Y1 - 2015/5/1
N2 - Background. With an increase in the use of colistin methansulfonate (CMS) to treat carbapenem-resistant Acinetobacter baumannii infections, colistin resistance is emerging. Methods. Patients with infection or colonization due to colistin-resistant A. baumannii were identified at a hospital system in Pennsylvania. Clinical data were collected from electronic medical records. Susceptibility testing, pulsed-field gel electrophoresis (PFGE), and multilocus sequence typing (MLST) were performed. To investigate the mechanism of colistin resistance, lipid A was subjected to matrix-assisted laser desorption/ionization mass spectrometry. Results. Twenty patients with colistin-resistant A. baumannii were identified. Ventilator-associated pneumonia was the most common type of infection. Nineteen patients had received intravenous and/or inhaled CMS for treatment of carbapenem-resistant, colistin-susceptible A. baumannii infection prior to identification of colistin-resistant isolates. The 30-day all-cause mortality rate was 30%. The treatment regimen for colistin-resistant A. baumannii infection associated with the lowest mortality rate was a combination of CMS, a carbapenem, and ampicillin-sulbactam. The colistin-susceptible and-resistant isolates from the same patients were highly related by PFGE, but isolates from different patients were not, suggesting evolution of resistance during CMS therapy. By MLST, all isolates belonged to the international clone II, the lineage that is epidemic worldwide. Phosphoethanolamine modification of lipid A was present in all colistin-resistant A. baumannii isolates. Conclusions. Colistin-resistant A. baumannii occurred almost exclusively among patients who had received CMS for treatment of carbapenem-resistant, colistin-susceptible A. baumannii infection. Lipid A modification by the addition of phosphoethanolamine accounted for colistin resistance. Susceptibility testing for colistin should be considered for A. baumannii identified from CMS-experienced patients.
AB - Background. With an increase in the use of colistin methansulfonate (CMS) to treat carbapenem-resistant Acinetobacter baumannii infections, colistin resistance is emerging. Methods. Patients with infection or colonization due to colistin-resistant A. baumannii were identified at a hospital system in Pennsylvania. Clinical data were collected from electronic medical records. Susceptibility testing, pulsed-field gel electrophoresis (PFGE), and multilocus sequence typing (MLST) were performed. To investigate the mechanism of colistin resistance, lipid A was subjected to matrix-assisted laser desorption/ionization mass spectrometry. Results. Twenty patients with colistin-resistant A. baumannii were identified. Ventilator-associated pneumonia was the most common type of infection. Nineteen patients had received intravenous and/or inhaled CMS for treatment of carbapenem-resistant, colistin-susceptible A. baumannii infection prior to identification of colistin-resistant isolates. The 30-day all-cause mortality rate was 30%. The treatment regimen for colistin-resistant A. baumannii infection associated with the lowest mortality rate was a combination of CMS, a carbapenem, and ampicillin-sulbactam. The colistin-susceptible and-resistant isolates from the same patients were highly related by PFGE, but isolates from different patients were not, suggesting evolution of resistance during CMS therapy. By MLST, all isolates belonged to the international clone II, the lineage that is epidemic worldwide. Phosphoethanolamine modification of lipid A was present in all colistin-resistant A. baumannii isolates. Conclusions. Colistin-resistant A. baumannii occurred almost exclusively among patients who had received CMS for treatment of carbapenem-resistant, colistin-susceptible A. baumannii infection. Lipid A modification by the addition of phosphoethanolamine accounted for colistin resistance. Susceptibility testing for colistin should be considered for A. baumannii identified from CMS-experienced patients.
UR - http://www.scopus.com/inward/record.url?scp=84928902817&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=84928902817&partnerID=8YFLogxK
U2 - 10.1093/cid/civ048
DO - 10.1093/cid/civ048
M3 - Article
C2 - 25632010
AN - SCOPUS:84928902817
VL - 60
SP - 1295
EP - 1303
JO - Clinical Infectious Diseases
JF - Clinical Infectious Diseases
SN - 1058-4838
IS - 9
ER -