Department of Microbiology, Haukeland University Hospital, Bergen, Norway.
Department of Microbiology, Haukeland University Hospital, Bergen, Norway.
Clin Microbiol Infect. 2019 Aug;25(8):981-986. doi: 10.1016/j.cmi.2018.11.030. Epub 2018 Dec 21.
The view of pleural empyema as a complication of bacterial pneumonia is changing because many patients lack evidence of underlying pneumonia. To further our understanding of pathophysiological mechanisms, we conducted in-depth microbiological characterization of empyemas in clinically well-characterized patients and investigated observed microbial parallels between pleural empyemas and brain abscesses.
Culture-positive and/or 16S rRNA gene PCR-positive pleural fluids were analysed using massive parallel sequencing of the 16S rRNA and rpoB genes. Clinical details were evaluated by medical record review. Comparative analysis with brain abscesses was performed using metagenomic data from a national Norwegian study.
Sixty-four individuals with empyema were included. Thirty-seven had a well-defined microbial aetiology, while 27, all of whom had community-acquired infections, did not. In the latter subset, Fusobacterium nucleatum and/or Streptococcus intermedius was detected in 26 patients, of which 18 had additional facultative and/or anaerobic species in various combinations. For this group, there was 65.5% species overlap with brain abscesses; predisposing factors included dental infection, minor chest trauma, chronic obstructive pulmonary disease, drug abuse, alcoholism and diabetes mellitus. Altogether, massive parallel sequencing yielded 385 bacterial detections, whereas culture detected 38 (10%) and 16S rRNA gene PCR/Sanger-based sequencing detected 87 (23%).
A subgroup of pleural empyema appears to be caused by a set of bacteria not normally considered to be involved in pneumonia. Such empyemas appear to have a similar microbial profile to oral/sinus-derived brain abscesses, supporting spread from the oral cavity, potentially haematogenously. We suggest reserving the term 'primary empyema' for these infections.
由于许多患者缺乏基础肺炎的证据,因此将脓胸视为细菌性肺炎并发症的观点正在发生变化。为了进一步了解病理生理机制,我们对临床特征明确的患者的脓胸进行了深入的微生物特征分析,并研究了观察到的脓胸与脑脓肿之间的微生物相似性。
使用 16S rRNA 和 rpoB 基因的大规模平行测序对培养阳性和/或 16S rRNA 基因 PCR 阳性的胸腔积液进行分析。通过病历回顾评估临床详细信息。使用来自挪威全国性研究的宏基因组数据进行脑脓肿的比较分析。
共纳入 64 名脓胸患者。37 例有明确的微生物病因,而 27 例均为社区获得性感染,无明确病因。在后一组中,26 例患者检测到核梭杆菌和/或中间链球菌,其中 18 例患者有不同组合的兼性和/或厌氧菌。对于这一组,与脑脓肿有 65.5%的物种重叠;易感因素包括口腔感染、轻微的胸部创伤、慢性阻塞性肺疾病、药物滥用、酗酒和糖尿病。总共,大规模平行测序产生了 385 种细菌检测,而培养检测到 38 种(10%)和 16S rRNA 基因 PCR/Sanger 测序检测到 87 种(23%)。
一组脓胸似乎是由一组通常不被认为与肺炎有关的细菌引起的。这些脓胸似乎具有与口腔/鼻窦来源的脑脓肿相似的微生物特征,支持从口腔传播,可能是血源性的。我们建议将这些感染保留为“原发性脓胸”。