Colistin-resistant acinetobacter baumannii: Beyond carbapenem resistance

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

Research output: Contribution to journalArticle

129 Citations (Scopus)

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.

Original languageEnglish
Pages (from-to)1295-1303
Number of pages9
JournalClinical Infectious Diseases
Volume60
Issue number9
DOIs
Publication statusPublished - 01-05-2015
Externally publishedYes

Fingerprint

Colistin
Acinetobacter baumannii
Carbapenems
Acinetobacter Infections
Lipid A
Multilocus Sequence Typing
Pulsed Field Gel Electrophoresis
Ventilator-Associated Pneumonia

All Science Journal Classification (ASJC) codes

  • Microbiology (medical)
  • Infectious Diseases

Cite this

Qureshi, Z. A., Hittle, L. E., O'Hara, J. A., Rivera, J. I., Syed, A., Shields, R. K., ... Doi, Y. (2015). Colistin-resistant acinetobacter baumannii: Beyond carbapenem resistance. Clinical Infectious Diseases, 60(9), 1295-1303. https://doi.org/10.1093/cid/civ048
Qureshi, Zubair A. ; Hittle, Lauren E. ; O'Hara, Jessica A. ; Rivera, Jesabel I. ; Syed, Alveena ; Shields, Ryan K. ; Pasculle, Anthony W. ; Ernst, Robert K. ; Doi, Yohei. / Colistin-resistant acinetobacter baumannii : Beyond carbapenem resistance. In: Clinical Infectious Diseases. 2015 ; Vol. 60, No. 9. pp. 1295-1303.
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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.",
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Qureshi, ZA, Hittle, LE, O'Hara, JA, Rivera, JI, Syed, A, Shields, RK, Pasculle, AW, Ernst, RK & Doi, Y 2015, 'Colistin-resistant acinetobacter baumannii: Beyond carbapenem resistance', Clinical Infectious Diseases, vol. 60, no. 9, pp. 1295-1303. https://doi.org/10.1093/cid/civ048

Colistin-resistant acinetobacter baumannii : Beyond carbapenem resistance. / Qureshi, Zubair A.; Hittle, Lauren E.; O'Hara, Jessica A.; Rivera, Jesabel I.; Syed, Alveena; Shields, Ryan K.; Pasculle, Anthony W.; Ernst, Robert K.; Doi, Yohei.

In: Clinical Infectious Diseases, Vol. 60, No. 9, 01.05.2015, p. 1295-1303.

Research output: Contribution to journalArticle

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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

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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.

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Qureshi ZA, Hittle LE, O'Hara JA, Rivera JI, Syed A, Shields RK et al. Colistin-resistant acinetobacter baumannii: Beyond carbapenem resistance. Clinical Infectious Diseases. 2015 May 1;60(9):1295-1303. https://doi.org/10.1093/cid/civ048