大肠埃希菌下呼吸道感染的临床和药敏分析

目的：分析和总结大肠埃希菌下呼吸道感染的临床特点及抗生素敏感性的分布情况。方法：对40例大肠埃希菌下呼吸道感染的临床资料进行统计分析。采用纸片法（Kirby-Bauer)测定该菌的体外药物敏感性，若疑为ESBLs，则行确认试验。结果：40例中90％（36／40）患有基础疾病，其中慢性阻塞性肺疾病（COPD）合并呼吸衰竭最常见，70％（28／40）的患免疫功能低下，45％（18／40）入住ICU或CCU病房，22．5％（9／40）曾接受侵入性治疗，95％（38／40）前期使用过广谱抗生素，临床表现为发热（65％），咳嗽（92．5％），胸部X线多表现为双下肺淡薄斑片状阴影，药敏监测表明该菌广泛耐药，尤其是产ESBLs株。敏感率＞80％仅有亚胺培南／西司他丁，哌唑西林／他唑巴坦，头孢他啶，头孢吡肟，丁胺卡那。结论：大肠埃希菌下呼吸道感染多发在患有各种基础疾病，免疫功能低下，细菌耐药现象严重（尤其在产ESBLs的细菌中），治疗有赖于细菌培养和药物敏感试验结果。     

大肠埃希菌下呼吸道感染的临床和药敏分析

目的分析和总结大肠埃希菌下呼吸道感染的临床特点及抗生素敏感性的分布情况。方法对40例大肠埃希菌下呼吸道感染的临床资料进行统计分析。采用纸片法 (Kirby-Bauer)测定该菌的体外药物敏感性。若疑为ESBLs,则行确认试验。结果40例中90 % (36/40)患有基础疾病 ,其中慢性阻塞性肺疾病 (COPD)合并呼吸衰竭最常见 ,70 % (28/40)的患者免疫功能低下 ,45 % (18/40)入住ICU或CCU病房 ,22.5 % (9/40)曾接受侵入性治疗 ,95 % (38/40)前期使用过广谱抗生素。临床表现为发热 (65% )、咳嗽 (92.5 % )、咳痰 (80 % ) ,胸部X线多表现为双下肺淡薄斑片状阴影 ,药敏监测表明该菌广泛耐药 ,尤其是产ESBLs株。敏感率>80 %者仅有亚胺培南/西司他丁、哌唑西林/他唑巴坦、头孢他啶、头孢吡肟、丁胺卡那。结论大肠埃希菌下呼吸道感染多发在患有各种基础疾病、免疫功能低下者。细菌耐药现象严重 (尤其在产ESBLs的细菌中 ) ,治疗有赖于细菌培养和药物敏感试验结果     

大肠埃希菌感染及耐药性分析

目的:分析不同部位大肠埃希菌感染及其耐药情况。方法:药敏试验用K-B法,用WHO细菌耐药监测网提供的WHONET-4软件完成数据分析。结果:武汉科技大学附属天佑医院2007年10月～2009年9月临床分离的大肠埃希菌532株,泌尿道274株(51.5%)、伤口89株(16.7%)、呼吸道57株(10.7%)、引流及穿刺液44株(8.3%)、血液32株(6.0%)、其他36株(6.8%)。大肠埃希菌对亚胺培南、阿米卡星、头孢他啶、氨曲南、头孢噻肟及头孢唑林、头孢呋新的耐药率较低,对氨苄西林、复方磺胺、萘啶酸、哌拉西林、环丙沙星、四环素的耐药率在50%以上。泌尿道大肠埃希菌对头孢类、单环类抗生素的敏感性及对环丙沙星的耐药率显著高于其他部位。亚胺培南是治疗产β-内酰胺酶(ESBL)大肠埃希菌的首选药物。结论:大肠埃希菌感染部位不同,抗菌药物敏感性有差异,强调治疗大肠埃希菌感染须根据药敏试验合理选用抗生素。     

大肠埃希菌耐药性调查

目的:调查湖南省郴州地区大肠埃希菌的耐药性.方法:收集大肠埃希菌标本1 078株,菌株鉴定用常规双歧法,药敏试验用Kirby bauer法,并按1997年NCLLS标准判断结果.结果:大肠埃希菌的平均耐药率达40.6%,且大肠埃希菌对不同的抗菌药物的耐药率不相同.结论:大肠杆菌对头孢曲松、阿米卡星、卡那霉素的耐药率较低,可优先选用,选用其他抗菌药物时应先做药敏试验.     

外科感染大肠埃希菌耐药性变迁分析

随着抗菌药物的不合理使用,抗菌药物的耐药性快速上升,多重耐药、泛耐药菌及全耐药菌菌株不断增多[1]。本文对我院从外科临床标本中分离出的大肠埃希菌进行对比分析,报告如下。1资料与方法1.1菌株来源2011年1月至2013年12月我院从外科临床标本中共分离出大肠埃希菌297株,剔除同例患者相同部位的重复菌株。1.2方法病原学鉴定用VITEK-32自动分析系统;药敏试验采用K-B纸片扩散法,抗菌纸片由赛     

大肠埃希菌感染及药敏分析

目的了解大肠埃希菌感染情况及药敏现状,为临床医师合理使用抗生素提供依据。方法大肠埃希菌分离鉴定按《全国临床检验操作规程》进行,采用法国梅里埃阴性杆菌专用药敏鉴定板进行药敏试验。结果我院大肠埃希菌对12种常见抗生素的耐药率较高,其中以头孢噻吩最高,为84.3%,且对亚胺培南亦发现有耐药菌株（1例）。结论大肠埃希菌的耐药情况比较严重,医院应加强监测工作。     

357株大肠埃希菌耐药性监测

目的 对本院近3年大肠埃希菌进行常用抗生素的耐药监测及产ESBLs检出率进行比较分析.方法 药敏实验和双纸片协同试验对我院 2004年～2006年临床分离的357株大肠埃希菌进行监测分析.结果 大肠埃希菌对氨苄西林、环丙沙星、左氧氟沙星的耐药率都在50%以上,对头孢呋辛、头孢噻肟、头孢曲松、头孢他啶、氨曲南、庆大霉素、阿米卡星的耐药率都在40%左右,对哌拉西林/他唑巴坦、头孢西丁、头孢吡肟耐药率为20%左右,对碳青霉烯类抗菌药物亚胺培南/西司他丁、美罗培南全部敏感.大肠埃希菌ESBLs检出率 2004～2006年分别为 36.5%、38.7%、41.6%.结论 大肠埃希菌对绝大部分抗菌药物的耐药率均逐年增加,大肠埃希菌产ESBLs率呈逐年上升的趋势,积极加强耐药监测,合理、规范选用抗菌药物,才能控制耐药菌株的出现和传播.     

泌尿系统感染大肠埃希菌的耐药性分析

目的：了解焦作地区泌尿系统感染大肠埃希菌的耐药状况,为临床合理使用抗生素提供依据。方法收集临床中段尿标本培养分离的大肠埃希菌128株,用珠海迪尔全自动微生物分析仪进行细菌鉴定及药敏试验,应用WHONET5.5统计数据。结果128株尿液大肠埃希菌中,产ESBLs株检出率为65.6%,对多种抗生素都有不同程度耐药性。结论大肠埃希菌耐药率高,对其进行耐药监测,意义重大。     

295株大肠埃希菌的耐药性分析

目的 探讨大肠埃希菌的耐药性.方法 采用头孢西丁、头孢噻肟、头孢他啶、头孢呋辛、头孢吡肟、哌拉西林、环丙沙星、阿米卡星、丁胺卡那霉素和亚胺培南共10种抗菌药物对本院临床分离的295株大肠埃希菌的耐药性进行检测分析.结果 295株大肠埃希菌中检出产ESBLs菌株105株,检出率为35.6%.产ESBLs菌株和非产ESBLs菌株对亚胺培南均敏感、没有耐药株,对丁胺卡那霉素的耐药率无显著性差异(P>0.05).产ESBLs菌株对其余8种抗菌药物的耐药率均高于非产ESBLs菌株,差异具有统计学意义(P<0.01或P<0.05).结论 产生ESBLs是导致大肠埃希菌多重耐药的重要原因.亚胺培南是治疗产ESBLs大肠埃希菌的首选药物.临床治疗时应根据药敏试验结果合理地使用抗菌药物,以减少耐药菌的产生.     

大肠埃希菌肠道外感染及其治疗的研究近况

大肠埃希菌是人类常见的肠道致病菌,其感染主要引起腹泻。但在一定条件下大肠埃希菌也可造成尿路、腹腔、胆道,肺部和血流感染等肠道外感染,且其临床表现因感染部位的不同而不同。抗菌治疗是大肠埃希菌肠道外感染的主要治疗措施,必要时还可予以手术治疗。本文主要就大肠埃希菌肠道外感染的临床表现及治疗予以综述。     

载铜蒙脱石及其杀灭大肠杆菌机制的研究

为制备载铜蒙脱石(Cu-MMT)并研究其杀菌活性及机制，采用离子交换法制得Cu-MMT，对其结构与表面特性进行表征。以大肠杆菌为试验菌株，检测Cu-MMT对细菌的最小抑菌浓度(MIC)和最小杀菌浓度(MBC)， Cu-MMT杀菌过程中菌液胞内酶活性的变化，并观察细菌形态。结果显示，载铜后蒙脱石的离子交换容量增大，但比表面积和表面负电荷密度下降；Cu-MMT对大肠杆菌的MIC和MBC分别为0.16和0.64 mg·mL^-1；Cu-MMT可使细菌细胞膜受损，胞内酶诸如冬氨酸氨基转移酶、乳酸脱氢酶和丙氨酸氨基转移酶等外泄。Cu-MMT对细菌具有较强的杀灭活性，其杀菌机制：Cu-MMT与细菌发生吸附作用，使细菌细胞膜形态和通透性改变，胞内物外泄而死亡。     

Essential oils—their antimicrobial activity against Escherichia coli and effect on intestinal cell viability

Essential oils are known to possess antimicrobial activity against a wide spectrum of bacteria. The main objective of this study was to evaluate possible harmful effects of four commonly used essential oils and their major components on intestinal cells. Antimicrobial activity of selected plant extracts against enteroinvasive Escherichia coli was dose dependent. However, doses of essential oils with the ability to completely inhibit bacterial growth (0.05%) showed also relatively high cytotoxicity to intestinal-like cells cultured in vitro. Lower doses of essential oils (0.01%) had only partial antimicrobial activity and their damaging effect on Caco-2 cells was only modest. Cell death assessment based on morphological and viability staining followed by fluorescence microscopy showed that essential oils of cinnamon and clove and their major component eugenol had almost no cytotoxic effect at lower doses. Although essential oil of oregano and its component carvacrol slightly increased the incidence of apoptotic cell death, they showed extensive antimicrobial activity even at lower concentrations. Relatively high cytotoxicity was demonstrated by thyme oil, which increased both apoptotic and necrotic cell death incidence. In contrast, its component thymol showed no cytotoxic effect as well as greatly-reduced ability to inhibit visible growth of the chosen pathogen in the doses used. On the other hand, the addition of all essential oils and their components at lower doses, with the exception of thyme oil, to bacterial suspension significantly reduced the cytotoxic effect of E. coli on Caco-2 cells after 1 h culture. In conclusion, it is possible to find appropriate doses of essential oils showing both antimicrobial activity and very low detrimental effect on intestinal cells.     

亚抑菌浓度抗菌药物对细菌耐药和致病性的影响

由于药物吸收、分布和代谢过程的存在,抗菌药物治疗过程中不可避免地出现抗菌药物浓度低于感染细菌最低抑菌浓度的情况,即处于亚抑菌浓度。研究表明亚抑菌浓度的抗菌药物虽不能杀灭细菌,但可影响细菌耐药、黏附、运动和毒素的释放等生物学效应,该效应具有菌株特异性和药物特异性。亚抑菌浓度可改变细菌的致病性并影响临床感染的治疗结果,具有重要的临床意义,综述亚抑菌浓度的抗菌药物对细菌耐药和细菌致病性的影响,以期为相关研究提供参考。

     

Proteomic analysis of zearalenone toxicity on mouse thymic epithelial cells

Zearalenone (ZEA) is one of the most major food contaminants in cereal crops worldwide, risking health of both livestock and humans. This study aimed to assess the cytotoxicity and the underlying mechanism of ZEA on thymic epithelial cells. By using proteomics analysis, we identified 596 differentially expressed proteins in MTEC1 cells upon zearalenone exposure, of which 245 were upregulated and 351 were downregulated. Gene ontology (GO) analysis suggested that differentially expressed proteins were participated in protein synthesis, oxidative phosphorylation, and ATP binding. KEGG pathway enrichment analysis showed that differentially expressed proteins were mainly related to mitochndrial metabolism, such as citrate cycle (TCA cycle) and oxidative phosphorylation. We demonstrated that ZEA treatment was able to increase the intracellular reactive oxygen species (ROS) level, to decrease ΔΨm, ATP level, and the copy number of mtDNA, leading to necrotic cell death. Moreover, we showed that ZEA treatment inhibited cell proliferation and induced G2/M phase arrest by downregulation of proliferation-associated proteins ERK, p-ERK, CDK1, and p-CHK1. Taken together, we found that the toxicity of ZEA on thymic epithelial cells is mainly caused by the inhibition of mitochondrial dysfunction and cell proliferation. Our study might open new avenues for treatment strategies.     

Another look at differences in the susceptibility of Escherichia coli and Klebsiella pneumoniae to cephalothin and cefazolin

The significance of in vitro susceptibility tests on Enterobacteriaceae to cephalothin and cefazolin has not been exactly defined in the guidelines of the National Committee for Clinical Laboratory Standards. In the hope of clarifying this confusion, we provide additional information from an ancillary study of the Taiwan Surveillance of Antimicrobial Resistance 1998 (TSAR I). There were 505 Escherichia coli and 227 Klebsiella pneumoniae isolates susceptible to cephalothin, reported by 42 participating hospitals. The susceptibility of these isolates were re-tested at the Microbial Infections Reference Laboratory using cefazolin, with the result that 72% of the 252 cephalothin-resistant E. coli isolates and 24% of the 41 cephalothin-resistant K. pneumoniae isolates were found to be susceptible to cefazolin. We further surveyed the availability of cephalothin and cefazolin in Pharmacy Departments; all of the TSAR I hospitals had cefazolin available in their pharmacies. The resistance rate of E. coli was significantly lower for 12 hospitals that had cefazolin in both pharmacy and laboratory compared with 11 hospitals that had cefazolin available in pharmacy but cephalothin in laboratory. In addition, for all the hospitals that had cephalothin available for clinical use, the resistance rate was twice as low in two hospitals reporting cefazolin susceptibility as in the seven hospitals reporting cephalothin susceptibility. Our findings suggest that inappropriate selection of cephalothin and cefazolin for susceptibility testing contribute to inaccurate indications of in vivo activity for first generation cephalosporins in the treatment of E. coli infections.     

木樨草素对小鼠实验性溃疡性肠炎影响

目的：观察木樨草素对小鼠急性结肠炎的药效作用。方法：2，4-二硝基氯苯(DNCB)／乙醇灌肠制作小鼠急性结肠炎模型，灌肠给予木樨草素(1、10、50mg·kg~(-1))，考察木樨草素对小鼠结肠黏膜组织形态损伤，以及结肠组织髓过氧化物酶(MPO)活力和前列腺素E_2(PGE_2)含量等的影响。结果：DNCB诱发结肠炎后，小鼠出现腹泻、充血、溃疡、肠壁增厚等变化。灌肠给予木樨草素后，对小鼠的腹泻、组织损伤等有显著改善，并且能够降低结肠组织中MPO活性和pGE_2的含量。结论：木樨草素抑制炎性浸润、渗出和组织增生，减轻结肠黏膜的病理损害，对实验性动物急性结肠炎有较好的治疗作用。     

鸡肝散药效成分木犀草素在大鼠体内的药代动力学

建立RP-HPLC法测定大鼠灌胃鸡肝散提取物后血浆中木犀草素的含量，并研究木犀草素在大鼠体内的药代动力学行为。大鼠灌胃鸡肝散提取物后，血浆样品经三氯乙酸沉淀蛋白，用RP-HPLC法测定。血浆中木犀草素的线性范围为0.37～47.27 μg·mL^-1；定量限为0.37 μg·mL^-1；方法回收率93%～99%，提取回收率75%～85%，日内及日间精密度均小于5%。鸡肝散提取物在大鼠体内的药代动力学行为符合开放二室模型。经大鼠性别和测定时间两因素方差分析，提示不同性别的大鼠的血药浓度具有显著性差异。通过质谱法鉴定了血浆中代谢物为葡糖醛酸结合物。建立的大鼠血浆中木犀草素的含量测定方法具有灵敏、准确，专属性强等特点，可用于鸡肝散药效成分木犀草素的体内药代动力学研究。     

抗菌药物使用强度对大肠埃希菌耐药性的影响

目的 分析大肠埃希菌常用抗菌药物耐药率与抗菌药物使用强度的相关性,为耐药菌的防控和治疗提供依据。方法 采用回顾性调查分析方法收集汕头大学医学院第一附属医院2013-2017年抗菌药物的使用强度和大肠埃希菌的耐药率,采用Pearson统计方法进行使用强度与耐药率的相关性分析。结果 抗菌药物使用强度排前5名的是左氧氟沙星、头孢他啶、莫西沙星、头孢曲松和哌拉西林舒巴坦,分别为11.46,3.76,2.75,2.21,1.95;对大肠埃希菌耐药率<10%的是亚胺培南西司他丁、哌拉西林他唑巴坦、头孢替坦、呋喃妥因和阿米卡星,耐药率>80%的是氨苄西林和头孢唑林,其余大部分被检测药物耐药率主要集中在50%左右,呈中等耐药;抗菌药物使用强度与耐药率的相关分析发现,亚胺培南西司他丁、头孢他啶和庆大霉素的耐药率与其使用强度呈显著的正相关性。结论 大肠埃希菌的耐药率与部分抗菌药物的使用强度存在显著的相关性,合理控制抗菌药物的使用强度是改善耐药率的有效途径之一。     

臭氧应激对人支气管上皮细胞上皮钙粘素表达的影响

目的：观察人支气管上皮细胞（human bronchial epithelial cells，HBECs）上皮钙粘素（E—cadherin，E-cd）的表达，探讨E—cd在维持气道损伤修复过程中的变化及意义。方法：分别采用免疫细胞化学染色和RT—PCR的方法检测HBECs E—cd及HBECs E—cd mRNA的表达。结果：臭氧（ozone，O3）应激可使HBECs膜上E—cd的表达减少，胞浆内E—cd表达增加（P〈0．05）。随着O3应激停止后的时间延长，膜上E—cd表达逐渐增加，胞浆内E-cd表达则减少。在停止O3应激后的第32h E—cd的表达恢复正常。O3应激对HBECs E—cd mRNA的表达无明显影响（P〉0．05）。结论：HBECs有E—cd表达，O3应激影响HBECs E—cd的分布。     

Diesel exhaust enhances influenza virus infections in respiratory epithelial cells.

Several factors, such as age and nutritional status, can affect the susceptibility to influenza infections. Moreover, exposure to air pollutants, such as diesel exhaust (DE), has been shown to affect respiratory virus infections in rodent models. Influenza virus primarily infects and replicates in respiratory epithelial cells, which are also a major targets for inhaled DE. Using in vitro models of human respiratory epithelial cells, we determined the effects of an aqueous-trapped solution of DE (DE(as)) on influenza infections. Differentiated human nasal and bronchial epithelial cells, as well as A549 cells, were exposed to DE(as) and infected with influenza A/Bangkok/1/79. DE(as) enhanced the susceptibility to influenza virus infection in all cell models and increased the number of influenza-infected cells within 24 h post-infection. This was not caused by suppressing antiviral mediator production, since interferon (IFN) beta levels, IFN-dependent signaling, and IFN-stimulated gene expression were also enhanced by exposure to DE(as). Many of the adverse effects induced by DE exposure are mediated by oxidative stress. Exposure to DE(as) used in these studies generated oxidative stress in respiratory epithelial cells, and addition of the antioxidant glutathione-ethylester (GSH-ET) reversed the effects of DE(as) on influenza infections. Furthermore, DE(as) increased influenza virus attachment to respiratory epithelial cells within 2 h post-infection. Taken together, the results presented here suggest that in human respiratory epithelial cells oxidative stress generated by DE(as) increases the susceptibility to influenza infection and that exposure to DE(as) increases the ability of the virus to attach to and enter respiratory epithelial cells.