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随着Colistin用于治疗碳青霉烯类敏感的鲍曼不动杆菌感染,细菌耐药显著上升。匹兹堡大学医学院的Yohei Doi博士团队发现,经过CMS(甲磺酸粘菌素)治疗后,碳青霉烯类敏感的鲍曼不动杆菌,几乎都会诱导产生耐药株。脂多糖A是耐药的重要机制,建议采用Colistin敏感性测试。Clin Infect Dis2015,60 (9).
http://weibo.com/p/1006063162502370/home?from=page_100606&mod=TAB#place
Colistin-Resistant Acinetobacter baumannii: Beyond Carbapenem Resistance- 1Division of Infectious Diseases, University of Pittsburgh School of Medicine, Pennsylvania
- 2Department of Microbial Pathogenesis, School of Dentistry, University of Maryland, Baltimore
- 3Clinical Microbiology Laboratory, University of Pittsburgh Medical Center, Pennsylvania
- Correspondence: Yohei Doi, MD, PhD, Division of Infectious Diseases, Department of Medicine, University of Pittsburgh School of Medicine, S829 Scaife Hall, 3550 Terrace St, Pittsburgh, PA 15261 (yod4@pitt.edu).
AbstractBackground. 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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