Résumé
Objective By detecting the distribution and homology analysis of Acinetobacter baumanii in the ICU ward,to con-trol nosocomial infection,provide theoretical basis to take effective measures.Methods From January 2016,20 patients in ICU of Shaanxi Provincial People's Hospital were taken into group.The samples of sputum and surrounding environment samples were cultured.The homology of Acinetobacter baumannii was analyzed by MALDI-Biotyper software,antimicrobial susceptibility test was analyzed by K-B.Results 27 strains of Acinetobacter baumannii were detected,mainly comes from sputum,hands of medical staffs and the environment,homology analysis results showed that the 27 strains of Acinetobacter baumannii was divided into two clusters(Ⅰtype 1 1 strains,Ⅱ type 1 6 strains),most of Acinetobacter baumannii were multi-resistant bacteria,except for the polymyxin B,minocycline and SCF.Conclusion The ways of transmission of Acineto-bacter baumanii in ICU were by medical personnel hand,pollution of the medical equipment and so on,strengthening the dis-infection and reasonable application of antimicrobial agents were taken advantageous for the prevention and control of acine-tobacter baumannii infection and transmission.
Résumé
In chicken fibroblast cell (CEF) cultures with antiserum against Newcastle disease virus (NDV) strain TZ060107, the virus was passed serially for 50 passages in 3 independent lineages. HN and F genes were amplified and sequenced every 10 passages. The derived virus A1-50 with most mutations among 3 lineages was further passed for another 50 passages in CEF with or without antiserum against A1-50, each in 3 independent lineages. Sequence comparisons for HN and F genes of 60, 70, 80, 90 and 100 passages indicated that the ratio of nonsynonymous mutations (NS) vs synonymous mutations (S) for HN genes in the lineages passed with antiserum against A1-50 was 5.25, which was obviously higher than 2. 375 of NS/ S in the lineages without the antiserum. The stable NS mutations occurred in the first 50 passages with the antiserum against the original TZ060107 were still maintained and one more new stable NS mutation appeared. For the F gene, 3 new stable NS mutations occurred during the second 50 passages in lineages with antiserum against A1-50 when the original NS mutations obtained in the first 50 passages with antiserum against TZ060107 still existed. Cross hemagglutination inhibition (HI) between original virus and its derivative viruses indicated that the more continuous passages in cell culture with antiserum passed, the bigger difference of antigenicity between the virus and the original virus had.