肺炎链球菌肺炎课件.ppt

坏死性肺炎（necrotizing pneumonia，NP ）,NP是一个病理学名称，与肺脓肿相同。 肺脓肿是细菌感染导致的肺实质坏死性病变，形成包含液化坏死物的脓腔 有临床学者将直径小于2 cm的肺内多发脓腔病变定义为NP或肺坏疽（pulmonary gangrene，PG） NP和肺脓肿的界定是人为的，大的空洞命名为肺脓肿，小的多发空洞则称为NP NP 具有影像学表现，可据此诊断。,影像学表现,X线片 肺部实变阴影内出现单发或多发小透亮区或肺大泡 CT 表现 肺部实变阴影内出现单个或多个低密度区域或空腔或肺大泡，无气液平面，增强CT显示没有边缘强化,病 例 1,男，1岁6月，因发热、咳嗽8天，呼吸困难2天入院。患儿体温波动于38.5-39.5，咳嗽逐渐加重，喉中有痰声，当地给予先锋霉素治疗1周，症状无好转，并出现呼吸困难。 胸部X线片和胸部CT提示左上下肺大片致密阴影，其内多发透亮区，左侧大量胸腔积液，有粘连包裹。 入院诊断左侧坏死性肺炎、胸腔积液。 白细胞:白细胞 22109/L, N:85% CRP: 180mg/L D-dimer 9.0/L(0.05-0.5),病 例 1,胸水检查提示为化脓性表现。胸水和痰液均培养出肺炎链球菌，确定肺炎、胸腔积液的病原菌为肺炎链球菌。 药敏实验（纸片法）提示对万古霉素敏感，青霉素不敏感。 给予头孢曲松治疗，转入外科经胸腔镜行胸腔积液引流、清创、胸膜剥脱术。 术后体温正常，继续治疗治疗3周出院。 出院后随访左侧肺炎部分吸收，多发透亮区逐渐消失，左侧肺部病变区域出现马赛克灌注，提示可能遗留感染后细支气管炎，目前仍在随访中。,病例 2,男，7岁，主因发热6天、咳嗽3天入院 2周前因发热、皮疹当地诊断麻疹，治疗后体温正常7天，6天前出现耳痛，诊断为中耳炎，次日再次出现发热，3天前耳痛消失，出现咳嗽，不重，痰少。 查体：体温正常，肺左下肺呼吸音降低，双肺无湿性罗音，外耳未见分泌物。 血常规：白细胞 27109/L, N:89% CRP: 120mg/L, 尿常规: 白细胞20-30/高倍,病例 2,胸部CT：双侧肺炎，伴少量胸腔积液痰液培养:肺炎链球菌，青霉素不敏感（纸片）血、尿培养阴性诊断：肺炎链球菌肺炎 中耳炎 泌尿系感染 败血症 治疗：头孢曲松，体温正常，1周咳嗽消失,欧洲多中心研究(Mark Woodhead, Chest 2019; 113:183s-187s),临床所见,痰液培养阳性(菌落100%), 1-4月份占痰液标本的45%左右, 目前阳性率下降,约占20-30% 重症肺炎链球菌肺炎近2年加重, 出现坏死性肺炎或肺脓肿、脓胸,肺炎链球菌坏死性肺炎,近年来，几个不同地区的研究均显示儿童肺炎链球菌NP有增多现象。 美国Tan等比较了单纯和复杂性肺炎链球菌肺炎（合并坏死、脓胸、肺炎旁胸腔积液或肺脓肿）病例分布，发现复杂性病例进行性增加，从1994年的22.6增加到2019年的53。英国Ramphul 等分析了2019年2月到2019年7月收治的75例儿童脓胸，15例伴有肺空洞性疾病，其中2000-2019占13例。,肺炎链球菌坏死性肺炎,台湾Hsieh等回顾分析表明国立台湾大学医院（NTUH）收治的71例儿童肺炎链球菌肺炎中40例（56.3）表现为复杂性肺炎.复杂性肺炎占肺炎链球菌肺炎的比率从2019年到2019年明显升高（2019年25，2019年70）.,复杂性肺炎的发生机制,肺炎链球菌不产生坏死毒素，它导致NP的机制不清。研究表明肺炎链球菌3型在成人经常引起肺组织化脓坏死，Hammond等认为这与其具有大量的荚膜多糖抗原，抵抗吞噬有关。,复杂性肺炎与血清型有关？,Tan等报道引起肺炎的肺炎链球菌血清型以6B、14和19F为主，1型容易引起复杂性肺炎 Ramphul 等检测了11例儿童脓胸合并空洞性疾病病例肺炎链球菌的细菌血清型，4例1型，3例3型，2例14型，2例为9V型。 Heish等检测38个菌株进行了血清型分型，14型最为常见，但血清型的分布在两组间并没有差异,复杂性肺炎与血清型有关？,五家医院常见的4种型19F、19A、23F和6B 19F明显较往年增加.,复杂性肺炎与耐药有关?,肺炎链球菌青霉素耐药和敏感性降低也是引起复杂性肺炎的原因？ Heish等检测了50株分离于肺炎病例的肺炎链球菌的MIC，青霉素不敏感或头孢曲松不敏感菌株在大叶性和复杂性肺炎病例的分布没有差异。,复杂性肺炎与毒力有关,还有学者认为肺炎链球菌导致坏死病例增多与细菌毒力增强有关肺炎链球菌毒力因子的变异有可能导致肺清除细菌的能力下降，从而进展为肺组织坏死。,坏死性肺炎与其他机制?,Hsieh等对3例NP死亡病例进行了尸体解剖，大体观右肺中叶存在气肿、坏死和坏疽；坏疽区显示大面积的梗塞和坏死，右肺中叶肺动脉内有血栓。认为肺炎链球菌引起儿童NP，可能与儿童很少发生的血管栓塞和PG有关。,抗生素治疗,279株肺炎链球菌对8种抗菌药物的敏感性检测结果显示: 肺炎链球菌对青霉素的不敏感率为86.0，62.7处于中介水平，耐药23.3。 在检测的内酰胺类抗菌药物中，肺炎链球菌对阿莫西林还保持着很高的敏感性，敏感率为92.1。 75.3的菌株对头孢曲松敏感，仅有19.0的菌株对头孢呋辛敏感。 几乎全部菌株（99.6）对红霉素耐药。,抗 生 素,对万古霉素和氧氟沙星有很高的敏感率。值得注意的是在上海分离到1株万古霉素不敏感菌株 对亚胺培南的不敏感率为17.6，以中介株为主。,其他治疗,引流治疗 胸穿、闭氏引流、胸腔镜 闭氏引流的条件： 白细胞、LDH、糖含量抗凝治疗等,细菌性气道感染,背景 临床上,看到一些病例,持续咳嗽(3周以上),有痰,可伴有喘息,无发热、不伴有中毒症状，胸片和CT未见肺炎征象或存在纹理粗乱,小叶中性性结节、细支气管壁增厚、轻微或局限的支气管扩张等，肺部可有干性罗音、喘鸣音 小年龄组多见于气管、支气管不通畅（软化、狭窄、异物后）、病毒感染后、BO、哮喘、脑瘫等基础疾病；大年龄组无明显诱因。,细菌性气道感染,文献称细菌化脓性气道疾病（中心气道有脓性分泌物） 细菌性细支气管炎（ CT提示有细支气管炎表现，小叶中性性结节、细支气管壁增厚） 持续细菌性支气管炎：超过1个月 多误诊为哮喘、BO、病毒感染、免疫功能低下 常见细菌为肺炎链球菌， 需要抗生素治疗2-6周,Outcomes in children treated for persistent bacterial bronchitis,BACKGROUND: Persistent bacterial bronchitis (PBB) seems to be under-recognised and often misdiagnosed as asthma. METHODS: A retrospective chart review was undertaken of 81 patients in whom a diagnosis of PBB had been made. Diagnosis was based on the standard criterion of a persistent, wet cough for 1 month that resolves with appropriate antibiotic treatment. Thorax. 2019 Jan;62(1):80-4.,Outcomes in children treated for persistent bacterial bronchitis,RESULTS: The most common reason for referral was a persistent cough or difficult asthma. In most of the patients, symptoms started before the age of 2 years, and had been present for 1 year in 59% of patients. At referral, 59% of patients were receiving asthma treatment and 11% antibiotics. Haemophilus influenzae and Streptococcus pneumoniae were the most commonly isolated organisms. Over half of the patients were completely symptom free after two courses of antibiotics. Only 13% of patients required or =6 courses of antibiotics.,Chronic wet cough: Protracted bronchitis, chronic suppurative lung disease and bronchiectasis,Pediatr Pulmonol. 2019 , 43(6):519-31. The role of persistent and recurrent bacterial infection of the conducting airways (endobronchial infection) in the causation of chronic respiratory symptoms, particularly chronic wet cough, has received very little attention over recent decades other than in the context of cystic fibrosis (CF). This is probably related (at least in part) to the (a) reduction in non-CF bronchiectasis in affluent countries and, (b) intense focus on asthma. In addition failure to characterize endobronchial infections has led to under-recognition and lack of research.,Chronic wet cough: Protracted bronchitis, chronic suppurative lung disease and bronchiectasis,The article describes our current perspective of inter-related endobronchial infections causing chronic wet cough; persistent bacterial bronchitis (PBB), chronic suppurative lung disease (CSLD) and bronchiectasis. In all three conditions, impaired muco-ciliary clearance seems to be the common risk factor that provides organisms the opportunity to colonize the lower airway. Respiratory infections in early childhood would appear to be the most common initiating event but other conditions (e.g., tracheobronchomalacia, neuromuscular disease) increases the risk of bacterial colonization. Also misdiagnosis of asthma is common and the diagnostic process is further complicated by the fact that the co-existence of asthma is not uncommon. The principles of managing PBB, CSLD and bronchiectasis are the same. Further work is required to improve recognition, diagnosis and management of these causes of chronic wet cough in children.,Outcomes in children treated for persistent bacterial bronchitis,CONCLUSION: PBB is often misdiagnosed as asthma, although the two conditions may coexist. In addition to eliminating a persistent cough, treatment may also prevent progression to bronchiectasis. Further research relating to both diagnosis and treatment is urgently required.,谢谢！,