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Colistin-Resistant Acinetobacter baumannii: Beyond Carbapenem Resistance

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...

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Published in:Clinical infectious diseases 2015-05, Vol.60 (9), p.1295-1303
Main Authors: 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
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container_title Clinical infectious diseases
container_volume 60
creator 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
description 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.
doi_str_mv 10.1093/cid/civ048
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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.</description><identifier>ISSN: 1058-4838</identifier><identifier>EISSN: 1537-6591</identifier><identifier>DOI: 10.1093/cid/civ048</identifier><identifier>PMID: 25632010</identifier><language>eng</language><publisher>United States: Oxford University Press</publisher><subject>Acinetobacter baumannii - drug effects ; Acinetobacter baumannii - genetics ; Acinetobacter baumannii - isolation &amp; purification ; Acinetobacter baumannii - pathogenicity ; Acinetobacter Infections - complications ; Acinetobacter Infections - drug therapy ; Acinetobacter Infections - microbiology ; Acinetobacter Infections - mortality ; Adult ; Aged ; Aged, 80 and over ; Ampicillin - therapeutic use ; and Commentaries ; ARTICLES AND COMMENTARIES ; Bacterial infections ; Carbapenems - pharmacology ; Carbapenems - therapeutic use ; Colistin - pharmacology ; Colistin - therapeutic use ; CRE bacteria ; Drug resistance ; Drug Resistance, Multiple, Bacterial ; Drug use ; Electronic Health Records ; Electrophoresis, Gel, Pulsed-Field ; Ethanolamines - chemistry ; Female ; Gram-negative bacteria ; Humans ; Lipid A - chemistry ; Lipids ; Male ; Mass spectrometry ; Microbial Sensitivity Tests ; Middle Aged ; Multilocus Sequence Typing ; Pneumonia, Ventilator-Associated - drug therapy ; Pneumonia, Ventilator-Associated - microbiology ; Spectrometry, Mass, Matrix-Assisted Laser Desorption-Ionization ; Sulbactam - therapeutic use</subject><ispartof>Clinical infectious diseases, 2015-05, Vol.60 (9), p.1295-1303</ispartof><rights>Copyright © 2015 Oxford University Press on behalf of the Infectious Diseases Society of America</rights><rights>The Author 2015. Published by Oxford University Press on behalf of the Infectious Diseases Society of America. All rights reserved. For Permissions, please e-mail: journals.permissions@oup.com.</rights><rights>Copyright Oxford University Press, UK May 1, 2015</rights><rights>The Author 2015. Published by Oxford University Press on behalf of the Infectious Diseases Society of America. All rights reserved. For Permissions, please e-mail: . 2015</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c524t-f5421cd4e44cae555ff8ca9c020970f51627a3fa26a56a1ffccb997e88b0a0373</citedby><cites>FETCH-LOGICAL-c524t-f5421cd4e44cae555ff8ca9c020970f51627a3fa26a56a1ffccb997e88b0a0373</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.jstor.org/stable/pdf/26365261$$EPDF$$P50$$Gjstor$$H</linktopdf><linktohtml>$$Uhttps://www.jstor.org/stable/26365261$$EHTML$$P50$$Gjstor$$H</linktohtml><link.rule.ids>230,314,780,784,885,27924,27925,58238,58471</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/25632010$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Qureshi, Zubair A.</creatorcontrib><creatorcontrib>Hittle, Lauren E.</creatorcontrib><creatorcontrib>O'Hara, Jessica A.</creatorcontrib><creatorcontrib>Rivera, Jesabel I.</creatorcontrib><creatorcontrib>Syed, Alveena</creatorcontrib><creatorcontrib>Shields, Ryan K.</creatorcontrib><creatorcontrib>Pasculle, Anthony W.</creatorcontrib><creatorcontrib>Ernst, Robert K.</creatorcontrib><creatorcontrib>Doi, Yohei</creatorcontrib><title>Colistin-Resistant Acinetobacter baumannii: Beyond Carbapenem Resistance</title><title>Clinical infectious diseases</title><addtitle>Clin Infect Dis</addtitle><description>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. 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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.</abstract><cop>United States</cop><pub>Oxford University Press</pub><pmid>25632010</pmid><doi>10.1093/cid/civ048</doi><tpages>9</tpages><oa>free_for_read</oa></addata></record>
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source JSTOR Archival Journals and Primary Sources Collection; Oxford Journals Online
subjects Acinetobacter baumannii - drug effects
Acinetobacter baumannii - genetics
Acinetobacter baumannii - isolation & purification
Acinetobacter baumannii - pathogenicity
Acinetobacter Infections - complications
Acinetobacter Infections - drug therapy
Acinetobacter Infections - microbiology
Acinetobacter Infections - mortality
Adult
Aged
Aged, 80 and over
Ampicillin - therapeutic use
and Commentaries
ARTICLES AND COMMENTARIES
Bacterial infections
Carbapenems - pharmacology
Carbapenems - therapeutic use
Colistin - pharmacology
Colistin - therapeutic use
CRE bacteria
Drug resistance
Drug Resistance, Multiple, Bacterial
Drug use
Electronic Health Records
Electrophoresis, Gel, Pulsed-Field
Ethanolamines - chemistry
Female
Gram-negative bacteria
Humans
Lipid A - chemistry
Lipids
Male
Mass spectrometry
Microbial Sensitivity Tests
Middle Aged
Multilocus Sequence Typing
Pneumonia, Ventilator-Associated - drug therapy
Pneumonia, Ventilator-Associated - microbiology
Spectrometry, Mass, Matrix-Assisted Laser Desorption-Ionization
Sulbactam - therapeutic use
title Colistin-Resistant Acinetobacter baumannii: Beyond Carbapenem Resistance
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