2194例男性泌尿生殖道支原体检测及药敏分析

目的研究男性泌尿生殖系统炎症患者解脲脲原体(Uu)和人型支原体(Mh)感染及对抗菌药物耐药情况,以了解本地区男性支原体的感染流行状况并指导临床合理选择使用抗菌药物。方法采用支原体鉴定药敏试剂盒,对男性生殖道感染者进行支原体培养及药敏试验。结果 2 194份标本中检出支原体636例,阳性率为28.96%,其中解脲脲原体阳性率为22.59%,人型支原体阳性率为0.96%,解脲脲原体和人型支原体混合感染阳性率为5.42%。支原体对抗菌药物药敏结果显示,抗菌活性较高的是多西环素、普拉霉素、四环素和交沙霉素。结论Uu是男性泌尿生殖系统支原体感染的主要病原体。临床治疗支原体感染时应尽量根据药敏结果选择敏感药物。普拉霉素、多西环素、四环素和交沙霉素可作为本地区非淋菌尿道炎经验用药的首选药物,避免使用喹诺酮类药物。     

女性泌尿生殖道支原体感染及耐药性观察

目的了解女性泌尿生殖道感染患者解脲支原体(Uu)和人支原体(Mh)感染及耐药情况,指导临床合理应用抗菌药物。方法采用法国梅里埃公司生产的IST2支原体培养及药敏试剂盒,对932例女性泌尿生殖道感染患者进行培养及药敏试验。结果 932例患者中支原体阳性426例,总检出率45.7%,其中Uu阳性354例(37.9%),Mh阳性14例(1.5%),Uu+Mh阳性58例(6.2%);药敏结果表明,Uu与Mh对多西环素、交沙霉素、四环素较为敏感,Uu对环丙沙星、氧氟沙星耐药率较高,而Mh对克拉霉素、红霉素、阿奇霉素耐药率较高。结论女性泌尿生殖道支原体检出率较高,主要以Uu为主,Uu和Mh对多种抗菌药物耐药,应引起临床重视。     

绍兴地区男女泌尿生殖道支原体感染特点及药敏差异分析

目的 了解绍兴地区男女泌尿生殖道支原体属感染的特点,比较男女两性对几种抗菌药物的耐药情况的差异.方法 应用法国生物梅里埃公司MycoplasmaISI试剂盒对2010年1月至201 1年10月男女两性泌尿生殖道标本进行支原体培养及药敏试验,统计解脲脲支原体和人支原体的检出率及耐药情况.结果 共1722例泌尿生殖道感染病例中,支原体属阳性869例,总阳性率50.46％,其中单纯解脲脲原体(Uu)感染702例,单纯人型支原体(Mh)感染29例,Uu及Mh混合感染138例;714例男性中支原体阳性190例,阳性率26.61％,1008例女性中支原体阳性679例,阳性率67.36％;男性单纯Uu感染耐药率较高的主要是:环丙沙星(80.50％)、氧氟沙星(63.60％),女性单纯Uu感染耐药率较高的主要是:环丙沙星(91.97％)、氧氟沙星(73.72％)、红霉素(47.81％).男女两性单纯Uu感染对红霉素、阿奇霉素、克拉霉素和交沙霉素的敏感性差异有统计学意义(P＜0.05).结论 男女两性泌尿生殖道支原体感染以Uu为主,且两者对多种抗菌药物的敏感性具有显著性差异,临床应根据药敏结果合理选取使用抗菌药物.     

887例宫颈分泌物支原体培养及耐药性分析

目的 了解女性泌尿生殖道感染患者支原体感染及耐药情况.方法 采用生物梅里埃IST2试剂盒,对887例宫颈分泌物进行培养及药敏试验.结果 887例标本中检出Uu阳性401例(45.2％),Mh阳性4例(0.5％),Uu+Mh阳性137例(15.4％),共检出542例(61.1％).药敏结果表明,Uu与Mh对原始霉素、交沙霉素、强力霉素、四环素较为敏感,对环丙沙星耐药率最高.结论 女性泌尿生殖道Uu和Mh感染率很高,主要以Uu为主,Uu和Mh对多种抗菌药物耐药,其中以环丙沙星为最高,单纯Uu、Mh和Uu+ Mh的耐药率存在一定差异,治疗支原体感染首选交沙霉素、四环素.     

4103例泌尿生殖道支原体感染及药敏分析

目的通过分析泌尿生殖道支原体感染及药敏情况,为临床提供用药指导。方法采用支原体检测试剂盒进行支原体属培养和药敏试验。结果4103例患者标本中,检出支原体属1336株,总阳性率为32．56％;其中单一解脲脲原体（Uu）感染1227例,阳性率为91．84％;单纯人型支原体（Mh）感染15例,阳性率为1．12％;Uu＋Mh混合合感染94例,阳性率为7．04％。解脲脲原体对阿奇霉素、红霉素、交沙霉素、罗红霉素、米诺环素、强力霉素敏感性高;单纯人型支原体对交沙霉素、米诺环素、强力霉素敏感。结论泌尿生殖道支原体感染以Uu为主。支原体大多具有多重耐药性,临床治疗需根据药敏结果选药物。     

3类抗菌药物体外抗解脲脲原体和人型支原体的作用

目的比较四环素类、大环内酯类和喹诺酮类3类抗菌药物,对临床分离株解脲脲原体(Uu)和人型支原体(Mh)的抗菌作用,为临床用药提供参考依据.方法采用直接肉汤药盘法测定了临床标本中,195株Uu和1218株Mh对3类抗菌药物中的8种抗生素的敏感性.结果 195株Uu对四环素、多西环素、米诺环素、罗红霉素、阿齐霉素、交沙霉素、氧氟沙星和司帕沙星的敏感率,分别为21.0%、48.2%、39.5%、79.0%、88.7%、74.9%、28.2%和64.6%.118株Mh对四环素、多西环素、米诺环素、罗红霉素、阿齐霉素、交沙霉素、氧氟沙星、司帕沙星的敏感率分别为5.1%、33.9%、26.3%、0.0%、0.0%、89.8%、70.3%和64.4%.960例混合感染的Uu Mh,对交沙霉素最敏感(79.2%).结论泌尿生殖道支原体的药敏监测对指导临床治疗具有重要意义.     

2709例泌尿生殖道支原体培养及耐药性分析

目的对门诊2 709例病例的支原体培养标本进行泌尿生殖道解脲脲原体(Ureaplasma urealyticum,Uu)与人型支原体(Mycoplasma hominis,Mh)感染情况及耐药性的分析,为临床的诊断及治疗提供参考依据。方法采用商品化试剂盒对2 709例标本进行Uu、Mh半定量培养及药物敏感试验。结果 2 709例标本中总阳性率为56.15%,其中Uu占比39.87%、Mh占比8.08%、Uu和Mh共同阳性者占比8.19%,男性标本阳性率为47.78%、女性标本阳性率为66.26%。药敏结果显示,单独Uu感染者对喹诺酮类(5.00%~34.40%)、红霉素(42.80%)敏感率较低,而对四环素类(88.90%~95.00%)、交沙霉素(97.30%)敏感率较高。单独Mh感染者与Uu和Mh混合感染者耐药情况均较为严重,除四环素、强力霉素、交沙霉素、美满霉素敏感率在50%以上,对其余药物的敏感率均在50%以下。结论泌尿生殖道支原体感染以Uu感染为主,其中女性感染率高于男性;药敏结果显示感染者对四环素、强力霉素、交沙霉素、美满霉素敏感率较高,单独Mh感染者与Uu和Mh混合感染者耐药情况更为严重。     

女性泌尿生殖道标本支原体检测及体外耐药性分析

分析了长沙市女性泌尿生殖道解脲支原体(Uu)和人型支原体(Mh)感染的现状,分布及耐药情况。应用支原体培养药敏试剂盒,对476例女性泌尿生殖道分泌物标本进行Uu和Mh的检测和药敏试验。476份标本支原体总检出率为37.0%。Uu检出率26.0%;Mh检出率为3.0%;两者混和感染检出率为8.0%。感染年龄集中在20~30岁的年龄段。支原体对常见抗生素的耐药率11.9%~79.5%。支原体感染是女性泌尿生殖道常见的感染病原体,对支原体感染敏感的抗生素是多西环素和美满霉素。     

长沙地区1409例泌尿生殖道支原体感染者的感染状况及药敏分析

目的了解长沙地区普通人群泌尿生殖道支原体感染的现状及药敏情况,为临床合理用药提供依据。方法收集并回顾性分析湖南省人民医院1 409例门诊泌尿生殖道感染者的支原体培养鉴定结果及其药物敏感试验结果。结果 1 409例门诊样本中,支原体总阳性率为15.3%(215/1409);其中,解脲脲原体(Uu)和人型支原体(Mh)阳性率为11.5%和6.2%,单独感染Uu、单独感染Mh和混合感染Uu+Mh阳性率分别为9.1%、3.8%和2.4%;女性支原体阳性率为22.3%,明显高于男性的3.3%(χ~2=92.378,P0.01);药物敏感性较高的为强力霉素、美满霉素和交沙霉素,耐药性较高的有喹诺酮类和罗红霉素;女性感染者对交沙霉素和壮观霉素的敏感性高于男性,对其他药物的敏感性则明显低于男性。单独Uu感染者对各抗菌药物(环丙沙星和壮观霉素除外)的敏感性均高于单独Mh感染者,而混合Uu+Mh感染者则为药物敏感性最低的一组(对大部分药物的敏感性低于40%)。结论长沙地区普通人群泌尿生殖道支原体感染的阳性率总体较低,但耐药问题依然突出,临床用药时可把四环素类药物和交沙霉素纳入首选,同时依据感染者的性别、感染类型等选择适宜药物进行治疗。     

2006～2010年泌尿生殖道炎症患者支原体感染率检测与耐药性分析

目的 了解杭州市萧山区2006～ 2010年泌尿生殖道炎症患者支原体感染及耐药情况.方法 对4 023例泌尿生殖道炎症患者用支原体鉴定及药敏试剂盒进行支原体培养及药敏试验.结果 支原体总检出率为48.1％,女性检出率51.2％明显高于男性41.8％ (P ＜0.05).支原体培养阳性患者中Uu单独感染1701例(88.0％),Mh单独感染57例(2.9％),Uu+ Mh混合感染176例(9.1％),Uu单独感染明显高于Mh单独感染和Uu+ Mh混合感染(P＜0.05).5年间支原体阳性检出率从2006年的39.4％到2010年的58.1％逐年增高,感染模式观察期内无明显变化.支原体对交沙霉素、原始霉素和强力霉素均敏感(敏感率≥91.4％),对四环素、红霉素、氧氟沙星和环丙沙星的耐药率高,均大于50％.比较2006年至2010年各种支原体对9种药物的耐药率,除四环素外耐药率呈不同程度上升,四环素耐药率2007年和2008年较高,后逐年下降,2010年为53.5％.混合感染总体耐药率比Uu或Mh单独感染耐药率高.结论 泌尿生殖道炎症患者支原体感染Uu比较常见,且女性检出率显著高于男性.临床分离支原体大多具有多重耐药性,临床治疗需根据药敏结果加以选择.     

Prion infection

The prion infection is a conversion of host encoded prion protein (PrP) from its cellular isoform PrPC into the pathological and infectious isoform PrPSc; the conversion process was investigated by in vitro studies using recombinant and cellular PrP and natural PrPSc. We present a brief summary of the results determined with our in vitro conversion system and the derived mechanistic models. We describe well characterized intermediates and precursor states during the conversion process, kinetic studies of spontaneous and seeded fibrillogenesis and the impact of the membrane environment.     

Glutathione and infection

Background

The tripeptide γ-glutamylcysteinylglycine or glutathione (GSH) has demonstrated protective abilities against the detrimental effects of oxidative stress within the human body, as well as protection against infection by exogenous microbial organisms.

Scope of review

In this review we describe how GSH works to modulate the behavior of many cells including the cells of the immune system, augmenting the innate and the adaptive immunity as well as conferring protection against microbial, viral and parasitic infections. This article unveils the direct antimicrobial effects of GSH in controlling Mycobacterium tuberculosis (M. tb) infection within macrophages. In addition, we summarize the effects of GSH in enhancing the functional activity of various immune cells such as natural killer (NK) cells and T cells resulting in inhibition in the growth of M. tb inside monocytes and macrophages. Most importantly we correlate the decreased GSH levels previously observed in individuals with pulmonary tuberculosis (TB) with an increase in the levels of pro-inflammatory cytokines which aid in the growth of M. tb.

Major conclusions

In conclusion, this review provides detailed information on the protective integral effects of GSH along with its therapeutic effects as they relate to the human immune system and health.

General significance

It is important to note that the increases in the levels of pro-inflammatory cytokines are not only detrimental to the host due to the sequel that follow such as fever and cachexia, but also due to the alteration in the functions of immune cells. The additional protective effects of GSH are evident after sequel that follows the depletion of this antioxidant. This is evident in a condition such as Cystic Fibrosis (CF) where an increased oxidant burden inhibits the clearance of the affecting organism and results in oxidant-induced anti-protease inhibition. GSH has a similar protective effect in protozoans as it does in human cells. Thus GSH is integral to the survival of some of the protozoans because some protozoans utilize the compound trypanothione [T(SH)₂] as their main antioxidant. T(SH)₂ in turn requires GSH for its production. Hence a decrease in the levels of GSH (by a known inhibitor such as buthionine sulfoximine [BSO] can have adverse effects of the protozoan parasites. This article is part of a Special Issue entitled Cellular functions of glutathione.     

Burkholderia cenocepacia infection

Phagocytosis is an important component of innate immunity that contributes to the eradication of infectious microorganisms; however, successful bacterial pathogens often evade different aspects of host immune responses. A common bacterial evasion strategy entails the production of toxins and/or effectors that disrupt normal host cell processes and because of their importance Rho-family GTPases are often targeted. Burkholderia cenocepacia, an opportunistic pathogen that has a propensity to infect cystic fibrosis patients, is an example of a pathogenic bacterium that has only recently been shown to disrupt Rho GTPase function in professional phagocytes. More specifically, B. cenocepacia disrupts Rac and Cdc42 seemingly through perturbation of guanine nucleotide exchange factor function. Inactivation of Rac, Cdc42 and conceivably other Rho GTPases seriously compromises phagocyte function.