金黄色葡萄球菌致病毒素基因分布特性及与致病性的相关性

目的研究金黄色葡萄球菌(简称金葡菌)致病毒素基因的分布特性及与致病性的关系。方法对临床收集的80株金葡菌,采用头孢西丁纸片法检测耐甲氧西林金葡菌(MRSA),多重聚合酶链反应法检测致病毒素基因中毒休克综合征毒素-1(TSST-1)、杀白细胞毒素(PVL),分析TSST-1、PVL基因阳性金葡菌的临床分布特性及与致病性的相关性。结果 80株金葡菌中MRSA总检出率为58.8%,PVL基因阳性金葡菌在医院的分布范围较广,主要引起呼吸系统感染、化脓性感染,也可引起其他感染性疾病,严重的可导致败血症;TSST-1基因阳性的MRSA均PVL基因阳性,均取自重症监护室肺部感染和化脓性感染的患者。结论 MRSA已成为医院感染的重要致病菌,携带致病毒素基因TSST-1、PVL的金葡菌也占有一定的比例,在医院的分布范围较广,致病毒素基因TSST-1、PVL可增强MRSA的致病力,这增加了临床治疗难度。     

以金黄色葡萄球菌致病因素为靶点的免疫疗法研究进展

金葡菌是引起皮肤和软组织感染的主要病原菌,严重感染者可引起致命性的肺炎、血流感染、感染性心内膜炎以及化脓性关节炎和骨髓炎等。2011年中国CHINET细菌耐药性监测结果显示,临床分离的革兰阳性菌中金葡菌检出率最高,     

金黄色葡萄球菌耐药基因及致病毒素基因的研究

目的 研究金葡菌耐药基因及致病因子中毒休克综合征毒素-Ⅰ(TSST-Ⅰ)基因和杀白细胞毒素 (PVL) 基因的分布特征.方法 收集临床分离的74株金葡菌,PCR法检测毒素基因TSST-Ⅰ、PVL和mecA耐药基因.结果 74株金葡菌 PCR法对其行mecA基因检测,检出率为55.4% (41/74).PVL阳性菌株的分离率为29.7%(22/74),PVL阳性的MRSA为15株(15/41,36.6%), PVL阳性的MSSA为7株(7/33,21.2%),差异无统计学意义(P>0.05).TSST-Ⅰ基因检出率为6.8%, MSSA中未检出TSST-Ⅰ基因.结论 MRSA呈多重耐药性,易造成医院内暴发流行,携带PVL和TSST-Ⅰ的金葡菌其致病力更强,应加强医院感染控制,防止其播散流行.     

金黄色葡萄球菌肺炎的防治

金黄色葡萄球菌(简称金葡菌)肺炎系金葡菌所致的急性肺部感染。病情较严重,病死率较高。常伴有化脓性并发症。金葡菌肺炎的感染途径有两条,一是呼吸道感染,多继发于麻疹、流感等病毒感染后,或肺结核和肺癌患者。二是血源性感染,如皮肤毛囊炎、蜂窝织炎、痈、疖、伤口或手术感染等。20多年来,产生青霉素酶的金葡菌感染的治疗比较困难,成     

金黄色葡萄球菌耐消毒剂基因qacA的流行病学研究

目的 了解重庆医科大学附一院近年临床分离的金葡菌中,耐消毒剂基因qacA的流行情况,从而指导临床抗菌药物、消毒剂的合理使用.方法 选取有代表性的1价和2价化合物,检测126株金葡菌的MIC,阳性株用PCR法检测qacA基因型,采用CLSI推荐的30 μg头孢西丁纸片法进行MRSA鉴定.结果 临床分离的126株金葡菌中,12株qacA基因型呈阳性(阳性率为9.5%),52株为MRSA(其中qacA基因阳性率为17.3%).结论 临床分离的金葡菌中,qacA基因携带率较高.     

皮肤软组织及创伤感染金黄色葡萄球菌分离株的毒素基因检测

目的了解皮肤软组织及创伤感染的金葡菌携带的杀白细胞素(Panton—Valentine Leukocidin,PVL)基因、表皮剥脱性毒素(ETs)基因、中毒性休克综合征毒素-1(TSST-1)的tst基因的特点。方法对连续收集的皮肤软组织感染中分离的90株金葡菌,采用多重PCR同时检测金葡菌特异性16SrRNA基因、mecA基因、PVL基因,采用PCR法检测TSST-1及EtsA、B基因。结果金葡菌mecA基因阳性47株(占金葡菌52.2%)为耐甲氧西林金葡菌(MRSA)。有1株MRSA的EtsB基因阳性,1株MRSA的TSST-1阳性,有7株金葡菌携带PVL基因,其中3株为mecA基因阳性株(MRSA)。结论金葡菌可分泌多种毒素,携带PVL毒素的金葡菌常可以引起严重的侵袭性感染,尤其对产毒的MRSA感染引起足够的重视,是防控的重点。     

甲氧西林耐药金黄色葡萄球菌SCCmec耐药元件及其菌株间水平转移机制

<正>金黄色葡萄球菌(金葡菌)是人及动物正常菌群的重要组成成分。部分金葡菌可导致疾病,引起皮肤、黏膜等处的化脓性感染,甚至导致菌血症、中毒性休克综合征等危及患者生命的严重疾病,是医院感染和社区获得性感染的重要病原菌之一。自1961年出现以来,耐甲氧西林金葡菌(MRSA)的感染率逐年攀升[1]。据估计,2005年美国因MRSA     

76例金黄色葡萄球菌医院感染患者的临床分析

目的：探讨2006年本院金黄色葡萄球菌（金葡菌）医院感染患者的临床影响因素及耐药情况。方法：回顾本院被确诊为医院感染的住院患者，分析其中金葡菌医院感染患者的临床特点、病原菌分布及耐药情况；并将非金葡菌医院感染患者作为对照组．采用Kirbv—Bauer琼脂扩散测定病原菌对抗菌药物的敏感度，并对患者的性别、年龄构成、原发疾病、所在病区、诊疗经过、诱发因素等资料进行回顾性调查，并进行统计分析。结果：2006年本院共有金葡菌培养阳性标本495例次．确诊为医院感染者96例次，其中91例次（76例患者）病史资料完整，非金葡菌医院感染354例次。76例中死亡20例．占2006年本院金葡菌医院感染者的26.32％。性别、年龄对金葡菌医院感染的发生无显著影响，而金葡菌医院感染发病最多的病区为神经外科，占30．77％（28例次／91例次）。下呼吸道标本培养金葡萄阳性者占所有金葡菌医院感染者的79．16％。诱发金葡菌医院感染的因素为手术、留置导尿、深静脉穿刺等侵入性操作。金葡菌对万古霉素敏感率为98.90％。结论：2006年本院金葡菌医院感染以神经系统疾病住院患者高发，可能与其原发病重、一般情况差有关.金葡菌感染以呼吸道为主，最主要的诱发因素为手术.     

重复序列引物聚合酶链反应追踪金黄色葡萄球菌所致医院感染

目的 利用重复序列引物聚合酶链反应（rep-PCR）追踪我院一起由金葡菌所致的医院感染。方法 分离得到的50株金葡菌用PHOENIX-100微生物自动鉴定系统鉴定，苯唑西林-盐琼脂筛选MRSA表型；PCR检测其耐药基因mecA；rep-PCR作金葡菌基因分型。结果 50株金葡菌中，22株mecA阳性，其中19株分离自患者标本。采用rep-PCR，50株金葡菌均出现9～11条带的电泳图谱，从而可分成11个不同的基因型。结论 rep-PCR是一种快速、简便、可靠的基因分型方法，是在分子水平追踪医院感染病原菌较理想的工具。     

584株葡萄球菌的临床分布和药敏试验

葡萄球菌是最常见的化脓性球菌之一,是临床化脓性感染和院内感染的主要病原菌。为了解其临床分布和对抗生素的耐药程度,现将我院1987～1989年从临床标本中分离出的414株金黄色葡萄球菌(下称金葡菌)和170株表皮葡萄球菌(包括白色葡萄球菌和柠檬色葡萄球菌,下称表葡菌)的临床分布和药敏试验结果报告如下。1 材料与方法1.1 菌株的来源.从本院住院及门诊病例的标本中分离获得。分离鉴定方法按常规法进行。1.2 药敏试验.采用平皿纸片法,抗生素纸片系杭州微生物试剂厂生产。2 结果与讨论2.1 细菌的分布.从12种临床标本中共检出金葡菌     

Talking genes

The worlds of genetics and speech pathology intersect in several places: some communication disorders clearly have a genetic basis, and many genetic conditions or syndromes have an effect on speech and language. The rapid changes in the world of genetics present a challenge to health professionals in maintaining their knowledge of this field. This paper will introduce genetics terminology and concepts that are useful in understanding genetics. With particular reference to paediatric genetic conditions, three important points in relation to speech and genetics will be discussed: (i) common disorders such as specific language impairment, cleft lip/palate and dyslexia have a multifactorial basis; (ii) the study of rare single gene syndromes can further the understanding of more common multifactorial conditions, and (iii) many syndromes have a speech and language phenotype as an important feature of the condition. Speech-language pathologists play an important role in recognising these phenotypes and assisting in the process of syndrome diagnosis.     

金黄色葡萄球菌耐药基因及致病毒素基因的相关性研究

目的研究携带TSST-1和PVL基因的金黄色葡萄球菌耐药特点、分布特征及与致病性的关系。方法临床收集74株金黄色葡萄球菌,采用PCR法检测TSST-1、PVL和mecA基因,纸片扩散法进行17种抗菌剂的耐药性检测。结果 74株金黄色葡萄球菌中mecA基因检出率为55.4%,其中22株检出PVL基因(30.3%),PVL阳性的耐甲氧西林金黄色葡萄球菌(MRSA)为15株(36.6%),甲氧西林敏感的金黄色葡萄球菌(MSSA)为7株(21.2%),两者间差异无统计学意义(P>0.05)。5株金黄色葡萄球菌中检出TSST-1基因(6.3%),均为MRSA。MRSA耐药性严重,并呈多重耐药性,携带基因PVL和TSST-1的MRSA除对万古霉素敏感外,对其他抗菌剂均耐药。结论携带基因TSST-1和PVL的金黄色葡萄球菌耐药性及致病力更强,增加了临床抗感染治疗的难度。     

Human clock genes

Rhythmic variations in physiological and behavioural processes are mediated by both endogenous and exogenous factors. Endogenous factors include self-sustaining biological pacemakers or clocks which in the absence of strong external influences self-sustain periodic rhythms in such diverse physiological and psychological processes as core body temperature, food intake, cognitive performance and mood. Clocks with endogenous periods near or at 24 h (called circadian clocks from the Latin, circa dies, meaning about one day) have been documented from prokaryotes to single cell eukaryotes to multi-cellular, complex animals such as flies, rodents and humans. Over the past few years, a revolution in the understanding of the molecular basis of these clocks has led to the identification of a number of core clock genes and their proteins, and the development of elegant feedback models to explain the molecular gears of circadian clocks. At least eight human orthologs of mouse core clock genes have been identified, and polymorphisms in two of these, hClock and hPer2, have been implicated in human sleep disorders. Remarkably, knowledge of these core clock genes and the development of sophisticated reporter systems to monitor clock gene promoter activity have led to the astonishing observation that our body is actually composed of millions of cellular clocks and oscillators whose co-ordinated activity gives rise to pronounced daily, monthly, and seasonal rhythms in physiology and behaviour. An idea that is gaining favour is that our physical and mental well-being is probably determined by the appropriate phasing of these millions of cellular clocks with recurring, meaningful events in the environment.     

NIDDM susceptibility genes

Non-insulin dependent diabetes mellitus (NIDDM) is a heterogeneous disorder and both genetic and nongenetic factors are associated with the development of diabetes. Until now five genes (HNF-4 alpha, glucokinase, HNF-1 alpha, IPF-1 and HNF-1 beta), whose mutation can result in MODY, insulin and insulin receptor genes, and mitochondria DNA have been reported to be responsible for diabetes. Furthermore the mutations in some genes which work for insulin secretion or action also have been reported. This review discusses our current knowledge of these NIDDM susceptibility genes.     

Human clock genes

Rhythmic variations in physiological and behavioural processes are mediated by both endogenous and exogenous factors. Endogenous factors include self-sustaining biological pacemakers or clocks which in the absence of strong external influences self-sustain periodic rhythms in such diverse physiological and psychological processes as core body temperature, food intake, cognitive performance and mood. Clocks with endogenous periods near or at 24 h (called circadian clocks from the Latin, circa dies, meaning about one day) have been documented from prokaryotes to single cell eukaryotes to multi-cellular, complex animals such as flies, rodents and humans. Over the past few years, a revolution in the understanding of the molecular basis of these clocks has led to the identification of a number of core clock genes and their proteins, and the development of elegant feedback models to explain the molecular gears of circadian clocks. At least eight human orthologs of mouse core clock genes have been identified, and polymorphisms in two of these, hClock and hPer2, have been implicated in human sleep disorders. Remarkably, knowledge of these core clock genes and the development of sophisticated reporter systems to monitor clock gene promoter activity have led to the astonishing observation that our body is actually composed of millions of cellular clocks and oscillators whose co-ordinated activity gives rise to pronounced daily, monthly, and seasonal rhythms in physiology and behaviour. An idea that is gaining favour is that our physical and mental well-being is probably determined by the appropriate phasing of these millions of cellular clocks with recurring, meaningful events in the environment.     

Finding schizophrenia genes

Genetic epidemiological studies suggest that individual variation in susceptibility to schizophrenia is largely genetic, reflecting alleles of moderate to small effect in multiple genes. Molecular genetic studies have identified a number of potential regions of linkage and 2 associated chromosomal abnormalities, and accumulating evidence favors several positional candidate genes. These findings are grounds for optimism that insight into genetic factors associated with schizophrenia will help further our understanding of this disease and contribute to the development of new ways to treat it.