Dataset Information

Carbapenem Breakpoints for Acinetobacter baumannii Group: Supporting Clinical Outcome Data from Patients with Bacteremia.

ABSTRACT: The carbapenem breakpoints set by different organizations for Acinetobacter are discordant, but supporting clinical data are lacking. This study aimed to provide the first clinical outcome data to support the carbapenem breakpoints for Acinetobacter baumannii (Ab) group in patients with bacteremia. This study included 117 adults who received carbapenems for treatment of Ab group bacteremia in Taipei Veterans General Hospital over an 8-year period. We analyzed 30-day mortality rates among patient groups acquiring isolates with different carbapenem minimal inhibitory concentrations (MICs). The carbapenem MIC breakpoint derived from classification and regression tree (CART) analysis to delineate the risk of 30-day mortality was between MICs of ? 4 mg/L and ? 8 mg/L. Mortality rate was higher in patients acquiring isolates with carbapenem MIC ? 8 mg/L than ? 4 mg/L, by bivariate (54.9% [28/51] vs 25.8% [17/66]; P = 0.003) and survival analysis (P = 0.001 by log-rank test). Multivariate analysis using logistic regression and Cox regression models including severity of illness indices demonstrated that treating patients with Ab group bacteremia caused by isolates with a carbapenem MIC ? 8 mg/L with carbapenem was an independent predictor of 30-day mortality (odds ratio, 5.125; 95% confidence interval [CI], 1.946-13.498; P = 0.001, and hazard ratio, 2.630; 95% CI, 1.431-4.834; P = 0.002, respectively). The clinical outcome data confirmed that isolates with MIC ? 4 mg/L were susceptible to carbapenem, and those with MIC ? 8 mg/L were resistant in patients with Ab group bacteremia.

SUBMITTER: Lee YT

PROVIDER: S-EPMC5028070 | biostudies-literature | 2016

REPOSITORIES: biostudies-literature

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Carbapenem Breakpoints for Acinetobacter baumannii Group: Supporting Clinical Outcome Data from Patients with Bacteremia.

Lee Yi-Tzu YT Chiang Mei-Chun MC Kuo Shu-Chen SC Wang Yung-Chih YC Lee I-Hsin IH Chen Te-Li TL Yang Ya-Sung YS

PloS one 20160919 9

The carbapenem breakpoints set by different organizations for Acinetobacter are discordant, but supporting clinical data are lacking. This study aimed to provide the first clinical outcome data to support the carbapenem breakpoints for Acinetobacter baumannii (Ab) group in patients with bacteremia. This study included 117 adults who received carbapenems for treatment of Ab group bacteremia in Taipei Veterans General Hospital over an 8-year period. We analyzed 30-day mortality rates among patient ...[more]

PMID: 27644087

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Project description:IntroductionColonization of the respiratory tract by Acinetobacter baumannii has been established as an independent risk factor for bacteremia. However, within-host evolution of A. baumannii in bacteremia has not been extensively investigated.MethodsWe performed whole-genome sequencing to discover the evolutionary characteristics that accompany the transition from respiratory tract carriage to bloodstream infection in three patients with A. baumannii bacteremia.ResultsWithin-host genetic diversity was identified. A total of 21 single nucleotide variants (SNVs) were detected. Genic and intergenic evolution occurred particularly in secretion system, DNA recombination, and cell motility genes. Intergenic SNVs occurred more frequently compared to synonymous and non-synonymous SNVs, which indicated potential transcription or translation regulation. Non-synonymous mutations mostly occurred during the transition from respiratory tract carriage to bloodstream infection. Isolates of clonal complex 208 (CC208) had lower substitution rate with approximately 10-6 nucleotide substitutions per site year-1, compared with non-CC208 isolates (approximately 10-5). We found evidence for the occurrence of recombination in one patient. A total of 259 genes were found to be gained or lost during the within-host evolution, and 231 genes were only detected in one patient. Gene function annotation results suggested that most genes (71/259) were related to replication, recombination, and repair. Universal bloodstream specific genes were not found in all three patients, and only one putative membrane protein related gene was lost in two patients.ConclusionOur results indicated that within-host evolution of A. baumannii bacteremia was driven by mutations, gene content changes, and limited effect of recombination. Gene content diversity between different patients was identified, which suggested interplay of both host and pathogen factors in within-host genetic diversity. Secretion system-related genes showed higher frequency of genomic variations during the within-host evolution. Our findings enhanced our understanding of within-host evolution of A. baumannii bacteremia and provided a framework for discovering novel genomic changes and pathogenicity genes important for bacteremia, which will be validated in future studies.

Project description:BackgroundWith an increase in the use of colistin methansulfonate (CMS) to treat carbapenem-resistant Acinetobacter baumannii infections, colistin resistance is emerging.MethodsPatients 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.ResultsTwenty 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.ConclusionsColistin-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.

Dataset Information

Carbapenem Breakpoints for Acinetobacter baumannii Group: Supporting Clinical Outcome Data from Patients with Bacteremia.

Publications

Carbapenem Breakpoints for Acinetobacter baumannii Group: Supporting Clinical Outcome Data from Patients with Bacteremia.

Similar Datasets

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