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目的:以129位社区获得性肺炎(CAP)患者为研究对象,对肺炎支原体(MP)的感染状况以及肺炎支原体对临床常用的抗菌药物的敏感性及其对大环内酯类的耐药机制加以了解与分析探讨。方法:集中129例CAP患者,取急性期咽拭子标本,在进行肺炎支原体分离培养操作之后,再应用聚合酶链反应(PCR)的理论与方法对临床分离株进行分子鉴定工作;应用微量稀释法可以用来测定肺炎支原体对抗菌药物的最低抑菌浓度;为了与标准菌株MPFH(ATCC 15531)的基因序列展开对比分析,从而在真正意义上研究出大环内酯类的耐药机制,还需要利用23Sr RNA进行基因测序。结果:在129例CAP患者咽拭子标本中,一共分离出20株肺炎支原体,分离率达到15.50%;实验最终得出肺炎支原体对四环素类和氟喹诺酮类的抗菌药物有着较好的敏感性;大环内酯类抗菌药物中,耐药机制均为23Sr RNA的基因2063位点在试验中由A突变为G。结论:肺炎支原体对大环内酯类抗菌药物的耐药形式比较严峻,造成这一形式的主要机制是23Sr RNA基因位点突变。
OBJECTIVE: To investigate 129 cases of community acquired pneumonia (CAP) in our hospital and investigate their susceptibility to mycoplasma pneumonia (MP) and their susceptibility to commonly used antimicrobial agents and their mechanisms of resistance to macrolides To understand and analyze. Methods: A total of 129 patients with CAP were enrolled. Acute pharyngeal swab specimens were collected. After isolation and culture of Mycoplasma pneumoniae, the clinical isolates were identified by polymerase chain reaction (PCR) Method can be used to determine the Mycoplasma pneumoniae antibacterial antimicrobial minimum inhibitory concentration; in order to carry out a comparative analysis with the standard strain MPFH (ATCC 15531) gene sequence, and thus in the true sense of the macrolide resistance mechanisms 23Sr RNA needs to be used for gene sequencing. Results: Totally 20 strains of Mycoplasma pneumoniae were isolated from 129 throat swabs from CAP patients, the isolation rate was 15.50%. The results showed that Mycoplasma pneumoniae had good sensitivity to tetracyclines and fluoroquinolones. Macrolide antibiotics, the resistance mechanism is 23S rRNA gene 2063 site in the experiment from A to G mutation. Conclusion: Mycoplasma pneumoniae is more resistant to macrolide antibiotics. The main mechanism leading to this form is mutation of 23S rRNA gene.