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. 2015 May 1;60(9):1295-303.
doi: 10.1093/cid/civ048. Epub 2015 Jan 28.

Colistin-resistant Acinetobacter baumannii: beyond carbapenem resistance

Zubair A Qureshi  1 , Lauren E Hittle  2 , Jessica A O'Hara  1 , Jesabel I Rivera  1 , Alveena Syed  1 , Ryan K Shields  1 , Anthony W Pasculle  3 , Robert K Ernst  2 , Yohei Doi  1
Affiliations

Colistin-resistant Acinetobacter baumannii: beyond carbapenem resistance

Zubair A Qureshi et al. Clin Infect Dis. .

Abstract

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.

Keywords: Acinetobacter baumannii; carbapenem resistance; colistin resistance; lipid A; molecular typing.

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Figures

Figure 1.
Figure 1.
Pulsed-field gel electrophoresis dendrogram of colistin-resistant Acinetobacter baumannii isolates from 20 patients. The isolates were grouped into 9 clusters with a cutoff of 80%, demonstrating substantial diversity.
Figure 2.
Figure 2.
Comparison of matrix-assisted laser desorption/ionization–time of flight analysis of lipid A isolated from colistin-susceptible and -resistant Acinetobacter baumannii isolates from patient 2. Lipid A isolated from colistin-resistant strains produced an ion peak at a mass-to-charge ratio (m/z) of 2034 on mass spectrometry (bold arrow) that corresponds to modified lipid A with the addition of a phosphoethanolamine group. Thin arrows reveal ion at m/z 1910 that corresponds to the bisphosphorylated hepta-acylated lipid A of A. baumannii.
See this image and copyright information in PMC

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