列线图模型在肺炎支原体感染患儿中塑型性支气管炎发生的预测价值

目的：探究列线图模型在肺炎支原体肺炎（MPP）患儿中塑型性支气管炎（PB）发生的预测价值。方法：以2018年6月至2022年6月兰州市西固区人民医院儿科收治的MPP患儿246例为研究对象进行回顾性分析,根据患儿是否发生PB分为PB组（n =66）和非PB组（n =180）。通过单因素分析及多因素Logistic回归分析筛选变量,构建MPP患儿PB发生的列线图预测模型,再分别通过校准曲线评估预测模型的一致性,受试者工作特征（ROC）曲线评估预测模型的准确性,决策曲线分析（DCA）评估预测模型的临床价值。结果：与非PB组比较,PB组患儿热程、体温热峰、中性粒细胞百分比、白细胞介素-6、乳酸脱氢酶、D-二聚体、C-反应蛋白、低氧血症比例、应用糖皮质激素比例、肺不张比例、胸腔积液比例显著升高（P ＜0.05）,血小板显著降低（P ＜0.05）。多因素Logistic回归结果示,热程、体温热峰、肺不张、胸腔积液、中性粒细胞百分比、血小板、白细胞介素-6、乳酸脱氢酶是MPP患儿PB发生的影响因素。校准曲线结果示,列线图模型预测PB的发生概率与实际发生率的一致性较好。ROC曲线结果示,列线图模型的曲线下面积为0.925（95%CI =0.886～0.965,P ＜0.05）。DCA结果示,列线图模型具有较高的临床净获益率。结论：本研究通过热程、体温热峰、肺不张、胸腔积液、中性粒细胞百分比、血小板、白细胞介素-6、乳酸脱氢酶构建了MPP患儿PB发生的列线图预测模型,具有较好的一致性、准确性及临床应用价值。     

双歧杆菌三联活菌肠溶胶囊联合阿奇霉素序贯疗法治疗对肺炎支原体肺炎腹泻患儿胃肠炎症的调节作用

目的观察双歧杆菌三联活菌肠溶胶囊联合阿奇霉素序贯疗法治疗对肺炎支原体肺炎腹泻患儿胃肠炎症的调节作用。 方法将肺炎支原体肺炎伴腹泻的患儿106例均分为对照组和观察组。对照组采用阿奇霉素序贯疗法治疗,观察组在对照组基础上给予双歧杆菌三联活菌肠溶胶囊治疗。比较两组疗效和肠道菌群失调发生率。比较两组胃肠激素、降钙素原(PCT)、C反应蛋白(CRP)、中性粒细胞百分比(NEUT%)、嗜酸性粒细胞计数(EOS)水平。 结果观察组总有效率高于对照组(P＜0.05)。治疗后,两组胃肠激素和PCT、CRP、NEUT%、EOS较治疗前下降(P＜0.05),且观察组低于对照组(P＜0.05)。观察组肠道菌群失调发生率低于对照组(P＜0.05)。 结论双歧杆菌三联活菌肠溶胶囊联合阿奇霉素序贯疗法治疗可减轻肺炎支原体并腹泻肺炎患儿炎症反应,调节胃肠激素,降低患儿肠道菌群失调的发生。     

The role of pneumolysin in pneumococcal pneumonia and meningitis

Diseases caused by Streptococcus pneumoniae include pneumonia, septicaemia and meningitis. All these are associated with high morbidity and mortality. The pneumococcus can colonize the nasopharynx, and this can be a prelude to bronchopneumonia and invasion of the vasculature space. Proliferation in the blood can result in a breach of the blood-brain barrier and entry into the cerebrospinal fluid (CSF) where the bacteria cause inflammation of the meningeal membranes resulting in meningitis. The infected host may develop septicaemia and/or meningitis secondary to bronchopneumonia. Also septicaemia is a common precursor of meningitis. The mechanisms surrounding the sequence of infection are unknown, but will be dependent on the properties of both the host and bacterium. Treatment of these diseases with antibiotics leads to clearance of the bacteria from the infected tissues, but the bacteriolytic nature of antibiotics leads to an acute release of bacterial toxins and thus after antibiotic therapy the patients can be left with organ-specific deficits. One of the main toxins released from pneumococci is the membrane pore forming toxin pneumolysin. Here we review the extensive studies on the role of pneumolysin in the pathogenesis of pneumococcal diseases.     

Activity of telithromycin and seven other agents against 1034 pediatric Streptococcus pneumoniae isolates from ten central and eastern European centers

Objective  To test the activity of telithromycin against 1034 Streptococcus pneumoniae isolates from pediatric patients in ten centers from ten central and eastern European countries during 2000–2001, and to compare it with the activities of erythromycin A, azithromycin, clarithromycin, clindamycin, and quinupristin–dalfopristin.
Methods  The minimum inhibitory concentrations (MICs) of telithromycin, erythromycin A, azithromycin, clarithromycin, clindamycin, levofloxacin, quinupristin–dalfopristin and penicillin G were tested by the agar dilution method with incubation in air, and mechanisms of resistance to macrolides and quinolones were investigated.
Results  Strains were isolated from sputum, tracheal aspirates, ear, eye, blood, and cerebrospinal fluid. Among S. pneumoniae strains tested, 36% had raised penicillin G MICs (≥ 0.12 mg/L). Susceptibilities were as follows: telithromycin, quinupristin–dalfopristin and levofloxacin, ≥ 99%; clindamycin, 83%; and erythromycin A, azithromycin and clarithromycin, 78%. Of 230 (22.3%) erythromycin A-resistant S. pneumoniae strains, 176 (79.6%) had erm(B) , 38 (16.1%) had mef(A) , and 10 (4.3%) had mutations in 23S ribosomal RNA or in ribosomal protein L4. The rates of drug-resistant S. pneumoniae are high in all centers except Kaunas, Riga, and Prague.
Conclusion  Telithromycin had low MICs against all strains, irrespective of macrolide, azalide or clindamycin resistance. Ribosomal methylation was the most prevalent resistance mechanism among all resistant strains, except in Sofia, where the prevalence of the efflux mechanism was higher.     

肺炎衣原体对血管内皮细胞的感染及其对ICAM-1表达的影响

目的:观察肺炎衣原体对人脐静脉内皮细胞(HUVECs)的感染及其对细胞分泌和表达细胞间粘附分子1(ICAM-1)的影响,探讨C.pneumoniae感染在动脉粥样硬化形成中的作用及其可能机制。方法:用人喉表皮癌(HEP-2)细胞培养C.pneumoniae,以C.pneumoniae感染HUVE细胞,经透射电镜及PCR检测有无感染。用流式细胞仪检测感染前后HUVE细胞表面ICAM-1蛋白的表达的变化,用荧光定量RT-PCR检测ICAM-1mRNA的变化。结果:C.pneumoniae能感染体外培养的HUVE细胞;感染后12h,细胞表面ICAM-1蛋白的表达即增加,其峰值约在感染后24h;荧光定量RT-PCR结果显示其增加在mRNA水平。结论:C.pneumoniae能感染体外培养的人脐静脉内皮细胞并增加ICAM-1的表达,提示C.pneumoniae感染可能是动脉粥样硬化的始动因子之一,其致动脉粥样硬化机制可能与感染后血管内皮细胞粘附分子表达的增加有关。     

Monocyte cytokine secretion induced by chemically-defined derivatives of Klebsiella pneumoniae.

The capacity of a K. pneumoniae membrane proteoglycan (Kp-MPG) and four of its chemically defined derivatives to activate human monocytes was studied by measuring immunoreactive IL-1 beta, IL-6 and tumour necrosis factor-alpha (TNF-alpha) in culture supernatants. Monocyte culture supernatants were also tested for their comitogenic activity on concanavalin A-stimulated thymocytes and for their cytotoxic activity on the mouse fibroblastic L929 cell line. The four Kp-MPG derivatives were: (i) an acylpoly(1-3)galactoside (APG); (ii) an APG preparation submitted to acid hydrolysis which removed all fatty acids but left intact the galactose chain of APG (GC-APG); (iii) a preparation obtained by mild alkaline hydrolysis, containing additional ester-linked C14 and C16 fatty acids bound to the APG molecule (EFA-APG); and (iv) a polymer of the latter compound (APG pol). Kp-MPG induced the synthesis of IL-1 beta, IL-6 and TNF-alpha with dose-responses and kinetics similar to those of Salmonella minnesota lipopolysaccharide (Sm-Re-LPS). APG pol and EFA-APG induced the secretion of the three cytokines with lower potency than Kp-MPG or Sm-Re-LPS. APG did not trigger any detectable cytokine production and GC-APG induced only borderline and inconsistent responses. Our data demonstrate the critical role of ester-linked C14 and C16 fatty acids in the triggering of monocyte response to Kp-MPG derivatives.     

运用变性高效液相色谱对肺炎克雷伯菌产ESBL进行基因分型

目的 通过运用变性高效液相色谱（DHPLC）技术对前期研究已确认产超广谱β-内酰胺酶（ESBL）的肺炎克雷伯菌临床分离株TEM型质粒进行基因分型,试图建立一种方便快捷的用于ESBL分子诊断及其流行病学监测的新方法.方法 利用PCR技术从肺炎克雷伯菌临床分离株中扩增出TEM型质粒的编码序列,扩增产物运用DHPLC技术进行分析,分析提示,异常的样本通过测序确定其基因突变的类型,最后通过比对确定其基因型.结果 共分析了101例肺炎克雷伯菌临床分离株,全部样本均扩增出TEM型质粒的编码序列,经过DHPLC分析,52例（51.4%）样本表现为单一的洗脱峰,其形态与TEM-1标准菌株的峰型相一致,测序确定它们的碱基序列亦相一致,不存在变异,为TEM-1型;49例（48.6%）样本表现为异常的洗脱峰,它们均为双峰,形态一致,但异源双链峰的高度有差异,测序结果表明它们均存在四种相同的基因突变,在NCBI网站比对后确定为TEM-116;测序结果还提示,部分样本中TEM-1和TEM-116混合存在,其比例的不同表现为DHPLC时异源双链峰高度的差异;文献检索表明,本次确定的TEM-116为一新的基因亚型,为国内首次报道.结论 DHPLC具有简便快捷、高通量和自动化的特点,重复性好,不仅可对已知突变作出即时诊断,还可发现新的基因亚型,不失为一种较好的ESBL分子诊断方法及其流行病学监测手段.