Analysis of Bacterial Resistance in a Hospital during 2013 and 2015 / 中国药师

Objective: To analyze the distribution and drug resistance characteristics of clinical separation germ in a hospital from 2013 to 2015 to provide reference and basis for the prevention and control of nosocomial infection and rational use of antibiotics.Methods: The microbial susceptibility of isolated strains was detected using the conventional methods, and the drug sensitivity was analyzed by BioMerieux ATB 1.22.The drug sensitivity was determined according to CLSI 2014 criteria.Results: A total of 18 421 specimens were isolated during 2013 and 2015, and a total of 3 744 strains were isolated with the total positive rate of 20.32%.The separation and identification of pathogenic bacteria at the top 5 were Escherichia coli (967 strains, 44.34%), Bauman Acinetobacter (323 strains, 14.81%), Klebsiella pneumoniae (312 strains, 14.31%), Staphylococcus aureus (297 strains 13.62%) and Pseudomonas aeruginosa (282 strains, 12.92%).Besides the natural resistance of Klebsiella pneumoniae to amoxicillin, the resistance rate of Escherichia coli to piperacillin was over 75%, while the sensitivity rate of Klebsiella pneumoniae to piperacillin and tazobactam was more than 90%.The sensitivity of Acinetobacter baumannii and Pseudomonas aeruginosa to clinical antibiotics was basically below 40%, and the overall resistance level was higher than that of Bauman.MRSA was sensitive to nitrofurantoin, minocycline, quinupristin-Dafoe and leptin glycopeptide antibiotics (such as teicoplanin and vancomycin).Conclusion: The hospital should strengthen the monitoring of bacterial resistance and track the results in a timely manner so as to provide reference for the rational drug use in clinical practice.

Genetical diagnosis in a congenital achondroplasia family / 中华内分泌代谢杂志

Objective To indentify the gene mutation of fibroblast growth factor receptor 3 (FGFR3) gene in a Chinese family with congenital achondroplasia (ACH). Methods The genomic DNA from 2 clinically diagnosed ACH patients and the other 4 members from the same family was prepared for PCR. The products of PCR were purified and then sequenced directly. Results Two patients with ACH in this family showed G-A transition mutation at nucleotide 1138 as heterozygotes. Conclusion The G-A transition mutation at nucleotide 1138 in transmembrane domain of FGFR3 gene seems to be the pathologic cause of this Chinese family with ACH.