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Colistin resistance identifies carbapenem-resistant A. baumannii-treated patients
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Colistin-resistant Acinetobacter baumannii infection may be common among patients who have previously been treated with colistin methansulfonate for a carbapenem-resistant, colistin-susceptible strain of the bacterium, according to recent findings.
“Therapy of carbapenem-resistant A. baumannii infection often requires the use of colistin methansulfonate,” the researchers wrote. “Colistin methansulfonate is given intravenously as an inactive prodrug, which is converted in the blood to the active drug colistin sulfate. More recently, however, resistance to colistin has been reported among A. baumannii clinical strains.”
Researchers evaluated 20 patients colonized or infected with colistin-resistant A. baumannii at the University of Pittsburgh Medical Center between 2007 and 2014. The researchers reviewed records to extract data on patient demographics, underlying medical conditions, types of infection, antimicrobial drug exposure before and after isolation of colistin-resistant A. baumannii isolates, admission to the ICU, APACHE II score at the time of colistin-resistant infection, 30-day clinical outcomes and recurrence of infection within 90 days.
Concentrations of colistin methansulfonate (CMS) along with pulsed-field gel electrophoresis (PFGE) were determined, and multilocus sequence typing (MLST) assessed genetic relation and clonal lineages. The mechanism of colistin resistance was valued by subjecting lipid A to matrix-assisted laser desorption mass spectrometry.
In the 20 patients with colistin-resistant A. baumannii, ventilator-associated pneumonia was the most prevalent type of infection. Before identifying the colistin-resistant isolates, 19 of the patients had undergone intravenous and/or inhaled CMS to treat carbapenem-resistant, colistin-susceptible A. baumannii infection. A 30% rate of 30-day all-cause mortality was identified, with a combined regimen of CMS, carbapenem and ampicillin-sulbactam associated with the lowest rate of death.
PFGE found a significant degree of genetic relation between colistin-susceptible and colistin-resistant isolates from the same patients, but not between isolates from different patients, suggesting an evolution of resistance during CMS treatment. Additionally, MLST determined that all isolates belonged to the epidemic clonal lineage International Clone 2, and phosphoethanolamine modification of lipid A was responsible for colistin resistance.
“Colistin-resistant A. baumannii occurred almost exclusively among patients who had received CMS for treatment of carbapenem-resistant, colistin-susceptible A. baumannii infection,” the researchers wrote. “Lipid A modification was the mechanism underlying colistin resistance in all isolates. Susceptibility testing for colistin should be considered for A. baumannii identified from CMS-experienced patients.”
Disclosure: Qureshi reports no relevant financial disclosures. Please see the full study for a list of all other authors’ relevant financial disclosures.
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