婴幼儿感染性腹泻25例临床分析

婴幼儿感染性腹泻是婴幼儿常见病之一，近年来在病原学方面有明显变迁，以致病性大肠杆菌感染多见，据我院儿科１９８９年的统计结果表明，大肠艾希氏菌和克雷伯氏菌感染明显上升，病程长，病情重，应引起重视，本文就１９８９年１年的婴幼儿感染性腹泻的发病机制与病原学进行了分析。     

肺炎克雷伯杆菌肺炎50例临床分析

目的：了解肺炎克雷伯菌肺炎的发病现状和对抗生素的耐药性及其治疗。方法：采用回顾性分析我院于2001年1月－2002年6月住院肺炎克雷伯杆菌肺炎50例的发病，对抗生素耐药性及其治疗。结果：患多见于中老年男性，临床表现以发热、咳嗽、咳痰多见。结果：肺炎克雷伯杆菌对抗生素具有多重耐药性，耐药率为氨苄西林100％，替卡西林96％，阿莫西林／棒酸54％，头孢西丁46％，庆大霉素44％，培福沙星42％，头孢他定38％，未发现对亚胺培南的耐药菌株。结论：肺炎克雷伯杆菌肺炎临床表现无特殊性，亚胺培南对肺炎克雷伯杆菌的耐药率最低，应作为治疗重症肺炎克雷伯杆菌肺炎首选用药。     

肺炎衣原体感染小鼠肺组织免疫组化表现

目的 :通过研究小鼠肺组织免疫组化 ,对肺炎衣原体肺炎的发病机制进行初步的探讨。　方法 :以肺炎衣原体鼻内或静脉接种Icr小鼠 ,在不同时间点处死动物 ,用免疫组化的方法检测小鼠肺炎衣原体肺炎急性期肺组织的病理改变。　结果 :小鼠吸入肺炎衣原体后第 3、7、14天 ,肺组织中肺炎衣原体的免疫过氧化酶染色呈阳性。炎性肺组织阳性染色呈不均一性 ,为局限性分布。肺炎衣原体抗原阳性表达主要在肺泡巨噬细胞、间质细胞以及支气管周围淋巴组织等部位。静脉接种组引起上述类似改变 ,但程度轻 ,肺炎衣原体抗原阳性表达主要集中在肺泡巨噬细胞及间质细胞中。　结论 :免疫组化法检测小鼠肺炎衣原体肺炎急性期肺组织的病理改变 ,有助于肺炎衣原体肺炎急性期的诊断。肺炎衣原体呼吸道局部感染比血行感染的病理改变更为严重     

肺炎链球菌β-内酰胺酶TEM基因的发现

目的：探讨肺炎链球菌是否产β-内酰胺酶。方法：对2002年9月至2003年4月在苏州大学附属儿童医院就诊的呼吸道感染患儿痰标本中分离到的23株肺炎链球菌进行β-内酰胺酶TEM基因PCR检测与PCR扩增产物直接测序分析。结果：23株肺炎链球菌经TEM基因PCR检测21株阳性，阳性率达91．3％。测得1号菌株(SR001)基因序列为TEM-1型，已登录美国国立生物信息中心，注册号：AY392531。结论：从肺炎链球菌中检出β-内酰胺酶TEM基因。肺炎链球菌对青霉素耐药机制包括产β-内酰胺酶。     

RAPD法对肺炎克雷白杆菌的基因分型

为了探讨肺炎克雷白杆菌的基因分型，我们用煮沸法制备细菌基因组ＤＮＡ，进行随机引物－聚合物酶链反应，所有１８个肺炎克雷白杆菌菌株均产生了特异性的，可重复的扩增条带，提示：ＲＡＰＤ方法可用于肺炎克雷白杆菌的分型鉴定和进行分子流行病学研究。     

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。