The rapid expansion of carbapenem-resistant Acinetobacter baumannii (CRAB) clinical isolates is a big issue. We investigated the antibiotic susceptibility, molecular epidemiology and resistance gene of A. baumannii collected at two hospitals in Shanghai, China. Besides, the A. baumannii PCR-based replicon typing method (AB-PBRT) was conducted to categorize the plasmids into homogeneous groups on the basis of replicase genes. Most CRAB isolates showed high-level resistance to almost all antibiotics but retain susceptibility to colistin and tigecycline. A total of 101 isolates carried blaOXA-51-like gene. Sequencing identified the presence of blaOXA-66 for CRAB isolates. blaOXA–23 gene were discovered in all CRAB isolates. Each CRAB isolate contained 1–3 of 19 different plasmid replicase (rep) gene homology groups (GRs) and the GR6 (repAci6) was ubiquitous. Genotyping by Multilocus Sequence Typing (MLST) showed seven defined MLST patterns and three novel STs were found. eBURST analysis indicated they were all grouped in CC92 (GCII) with the most frequent ST208 (50%). Two blaOXA–23-bearing transposons were found: Tn2006 and Tn2008. Tn2008 were detected in 54 (96.4%) isolates and Tn2006 in two remaining isolates. The blaOXA–23 carbapenem gene was vitally associated with repAci6 plasmid belong to CC92 clonal group. Our survey revealed severe drug resistance in A. baumannii isolates. Tn2008-containing CC92 A. baumannii were endemic, which may facilitate the blaoxa23 dissemination.
Background: Ceftazidime-avibactam (CZA) has been approved in vitro activity against carbapenem-resistant K. pneumoniae (CRKP), but the experience for the treatment of CRKP in liver transplantation (LT) recipients was limited, and previous data on its efficacy in this setting are lacking. Methods: LT recipients with CRKP infection who received CZA treatment were reviewed retrospectively, microbiological and clinical response, adverse events were also assessed. The primary outcome was 30-day mortality after CZA administration. Results: CZA was used in 21 LT recipients (including 4 pediatric patients) with CRKP infections after failure with other antimicrobials. CZA was administered as monotherapy in 4 patients. Median time from the onset of CRKP infection until the initiation of CZA treatment was 2 days (IQR, 1– 6.5), and the median treatment duration was 12 days (IQR, 8.5– 18.5). The mortality at 14 days, 30 days and all-cause was 28.6%, 38.1% and 42.9%, respectively. In adult patients, clinical response of 14 days and 30 days was 70.6% (12/17) and 58.8% (10/17), respectively, while in pediatric patients the 14-day and 30-day clinical response were both 75%, respectively. The relapse rate during the treatment developed in 3 patients after 30 days with the cessation of CZA monotherapy. CZA resistance was not detected in any case and 3 (3/21, 14.3%) patients developed acute kidney injury related to uncontrolled infection. Conclusion: CZA shows promising results, even in monotherapy, for the treatment of patients with severe infections due to carbapenem-resistant K. pneumoniae among LT recipients. The emergence of resistance to CZA was not observed.