鼠疫的流行病学概述

鼠疫是由鼠疫耶尔森菌(Yersinia pestis)引起严重危害人类健康的烈性传染病。本文介绍了鼠疫病原体——鼠疫耶尔森菌的一般特性及生物学特性, 并对国内、外鼠疫疫情现状进行总结。目前鼠疫在全球范围内的流行已进入新的活跃期,世界卫生组织将鼠疫列为近20年来重新流行的急性传染病之一。当前,全球疫区主要分布在非洲、亚洲和南美洲。我国人间鼠疫自20世纪80年代开始处于明显回升势态,近10年流行逐渐下降,但防控形势依然艰巨。     

鼠疫传播动力学模型的构建研究

目的:采用疾病传播动力学模型描述鼠疫的流行特征,为科学地制定鼠疫的防控措施提供理论依据。方法:运用微分方程建立鼠间鼠疫和人间鼠疫的传播动力学模型,分析模型中各参数与疫情发展变化的关系。结果:使用基本繁殖率,平均鼠密度,感染者平均病死率,感染者平均治愈率等参数描述感染率随时间的变化趋势。结论:根据鼠间传播期、疫区传播期和人群扩散期的传播特点,分别开展各项防控工作,能够更好地控制鼠疫疫情。     

鼠疫——不可不防的传染病

前不久,青海省卫生厅正式对外公布,7月30日,青海省海南藏族自治州兴海县子科滩镇发现一起疑似鼠疫疫情,经实验室48小时细菌培养,结果呈现阳性。根据患者临床表现、流行病学调查和实验室检测结果,专家确认为肺鼠疫,确诊病例12例,其中首例病人（男性,牧民,32岁）死亡,其余11人主要为死者亲属,已在指定医院隔离治疗,病情稳定,救治效果明显。     

鼠疫

鼠疫是危害人类最严重的烈性传染病之一,仍是对人类生命健康、社会经济发展影响最为重要的公共卫生问题。阐述了世界和中国鼠疫自然疫源地的分布、动物鼠疫流行病学、中国鼠疫自然疫源地类型及动物流行病学特点、人类鼠疫流行病学和防治。     

新疆和田地区人蚤生态学的观察

人蚤(Pulex irritans Linnaeus,1758是一种广布于世界各地的多宿主寄生蚤。除叮咬和骚忧以破坏人类生活安定外,更重要的还是人类腺鼠疫的传播媒介,故有重要的流行病学意义。 新疆和田地区在历史上曾经发生过腺鼠疫的流行。该地人蚤数量极多,其季节消长与鼠疫流行有一定相关关系。为了更有效地防制人蚤的危害,我们在既往工作的基础上,于1980年3—9月对该地人蚤的生态学进行了比较详细的调查研究,结果如下:     

典型人兽共患病枚举

鼠疫鼠疫是鼠疫杆菌引起的一种烈性传染病,最先流行于鼠类及其他野生啮齿动物之间,借助鼠蚤叮咬而传染给人,也可以通过直接接触受感染的动物或被病兽咬伤而感染。病人死后皮肤会出现大片黑色瘀斑,因此又被人们称为"黑死病"。鼠疫通常有腺型、肺型和败血症型三种,病人发生肺部感染后,病原体可以借助飞沫传播。人类普遍易感,但病后可获得持久免疫。鼠疫传染性强、     

鼠疫疫苗研究的现状与展望

鼠疫（Plague）是由鼠疫耶尔森菌(Yersina pestis，Y. pestis)（简称鼠疫菌）引起的一种烈性传染病，属甲类传染病，具有高度传染性和致病性。在过去的鼠疫大流行中近2亿感染者死亡。疫苗接种是疾病预防控制的重要方法。现就鼠疫疫苗的研究进展作一综述，为新疫苗的研制提供参考。     

用遥感和地理信息系统研究传染病时空分布

和其他物种迁移或生物入侵过程类似, 传染病的时空传播与流行伴随着人类活动的全球化而加剧. 以血吸虫病时空传播流行定量模拟为例, 提出一种对已知传染源→媒介→宿主传播关系前提下的疾病传播的时空动态概念模型. 用西昌郊区血吸虫病流行区为例, 证明这类概念模型的可行性. 展示了遥感和地理信息系统在这类模型中具体的应用方法. 利用建立的模型, 模拟给不同村居民服药所达到的不同效果, 证明这类模型在传染病防治和控制中可以起到空间决策支持的作用. 本文介绍的模拟方法对鼠疫、肾综合征出血热、莱姆病等传染病有直接借鉴意义; 遥感和地理信息系统方法对其他有关的传染病, 甚至生物入侵过程的研究有所帮助.     

鼠疫减毒活疫苗研究现状与展望

鼠疫(plague)是由鼠疫耶尔森氏菌(Yersinia pesits)引起的烈性传染病,在人类历史上曾造成约2亿人的死亡,在我国被列为甲类传染病。由于鼠疫菌具有高度致病性、传染性,被列为最具潜力的生物战剂和生物恐怖剂。在面临鼠疫威胁时,疫苗是最为有力的武器。鼠疫疫苗研究中,减毒活疫苗是重要的研究方向,现就鼠疫减毒活疫苗的研究现状进行综述,为新疫苗的研制提供参考。     

西非埃博拉疫情对我国传染病防控体系能力建设的启示

通过回顾2014年在西非国家流行的埃博拉疫情,分析突发传染病大规模流行的主要原因和应急防控中面临的主要挑战,进一步从复杂系统的视角提出传染病防控体系框架,以及我国加强重大传染病防控能力建设的建议。     

鼠疫的发病机制研究进展

鼠疫是由鼠疫耶尔森菌(Yersinia pestis，Y. pestis)感染引起的一种人畜共患病。鼠疫在世界范围内出现过3次大流行，均引起致命的瘟疫。由于自然疫源面积不断扩大和人口流动愈加频繁，我国的鼠疫防治形势依旧严峻。本文就鼠疫耶尔森菌的毒力因子、对宿主细胞的黏附和侵袭、胞内繁殖、宿主内播散等机制的研究进展进行总结，有助于揭示鼠疫独特的致病和传播机制，为精准防治鼠疫提供工作基础。     

环介导等温扩增技术检测鼠疫耶尔森菌的敏感性和特异性研究

为观察环介导等温扩增(loop-mediated isothermal amplification,LAMP)技术能否适用于我国不同疫源地鼠疫耶尔森菌所有基因组型的检测,本研究建立了一种基于3a靶序列设计特异性引物快速检测鼠疫耶尔森菌的LAMP方法。选择分离自我国11个鼠疫自然疫源地的65株野生代表性鼠疫耶尔森菌株,同时以与其近源的假结核耶尔森菌、小肠结肠炎耶尔森菌及非近源的大肠埃希菌为对照菌株,观察其敏感性和特异性。结果显示,该LAMP方法与其他3种鼠疫耶尔森菌常规检测方法的结果一致。65株鼠疫耶尔森菌检测均为阳性,最低检出浓度为20个菌/μL;假结核耶尔森菌、小肠结肠炎耶尔森菌及大肠埃希菌标准菌株反应均为阴性。结果提示,本研究建立的LAMP技术对检测我国各疫源地鼠疫耶尔森菌具有高度特异性,且快速简便,无需特殊仪器,可肉眼判读结果,适用于野外现场鼠疫监测中的快速检测,在偏远地区疫情防控中具有实用价值。     

Comparative and evolutionary genomics of Yersinia pestis

Yersinia pestis is the causative agent of plague, causing three human plague pandemics in history. Comparative and evolutionary genomics of Y. pestis are extensively discussed in this review. Understanding the genomic variability and the adaptive evolution of Y. pestis from the genomic point of view will contribute greatly to plague detection, identification, control and prevention.     

Brief communication: co-detection of Bartonella quintana and Yersinia pestis in an 11th-15th burial site in Bondy, France

Historical and anthropological data suggest that skeletons excavated from an 11th to 15th century mass grave in Bondy, France, may be those of victims of the Great Plague. Using high-throughput real-time PCR investigation of the dental pulp collected from 14 teeth from five such skeletons, we detected Bartonella quintana DNA in three individuals and Yersinia pestis DNA in two individuals. DNA from five other deadly pathogens was not found. Suicide PCR genotyping confirmed Y. pestis DNA belonging to the Orientalis biotype. One individual had co-infection. These data suggest a plague epidemic in a population already infected by the body louse-transmitted B. quintana or a body louse-driven transmission of the plague that drove a medieval epidemic in inland Europe.     

DNA probe for detecting Yersinia pestis and serovariant I of Yersinia pseudotuberculosis by detecting specific DNA repeating sequences]

In order to construct a DNA probe for the plague pathogen detection, we have obtained the recombinant plasmid pRD100 carrying an EcoRI-flanked 140 bp fragment from the genetically silent region of Yersinia pestis species-specific plasmid pYP1. When used as a DNA probe for hybridization of DNA from various strains of 25 bacterial species, this DNA fragment was shown to have the complementary sequences in all investigated Yersinia pestis strains (200), including the plasmid pYP1 lacking ones, and in all the studied Yersinia pseudotuberculosis serotype I strains (80). The search for the probe target in these species has led us to conclusion that it is a specific repeated DNA sequence present in more copies in Yersinia pestis than in Yersinia pseudotuberculosis serotype I. The hybridization of these sequences with the radioactive probe and 24 hours autography makes possible the detection of 1.3 x 10(5) cells of Yersinia pestis and 3 x 10(6) cells of Yersinia pseudotuberculosis serotype I immobilized on the nitrocellulose membranes. Use of the probe for analysis of the nitrocellulose membrane fixed spleen smears from animals that died of experimental plague made possible the detection of Yersinia pestis cells within 48 h.     

No evidence of persistent Yersina pestis infection at prairie dog colonies in north-central Montana

Sylvatic plague is a flea-borne zoonotic disease caused by the bacterium Yersinia pestis, which can cause extensive mortality among prairie dogs (Cynomys) in western North America. It is unclear whether the plague organism persists locally among resistant host species or elsewhere following epizootics. From June to August 2002 and 2003 we collected blood and flea samples from small mammals at prairie dog colonies with a history of plague, at prairie dog colonies with no history of plague, and from off-colony sites where plague history was unknown. Blood was screened for antibody to Y. pestis by means of enzyme-linked immunosorbent assay or passive hemagglutination assay and fleas were screened for Y. pestis DNA by polymerase chain reaction. All material was negative for Y. pestis including 156 blood samples and 553 fleas from colonies with a known history of plague. This and other studies provide evidence that Y. pestis may not persist at prairie dog colonies following an epizootic.     

New records of sylvatic plague in Kansas

Sylvatic plague, or plague of wild rodents is caused by Yersinia pestis and entered California (USA) from Asia about 1899. Extensive sampling during the 1930's and 1940's documented the spread of plague to approximately its current distribution in North America. Records from the Centers for Disease Control and Prevention document plague in Kansas (USA) between 1945 and 1950, but since then there has been no documentation of plague in the state. Following a die-off of a black-tailed prairie dog (Cynomys ludovicianus) colony on the Cimarron National Grassland, in the southwestern corner of Kansas (3710'N, 10145'W), we sampled fleas from burrows in June 1997, and tested them for Yersinia pestis. Twelve of 13 pools of Oropsyla hirsuta and one of two Pulex sp. were positive. A similar sample of fleas, from another colony where black-tailed prairie dogs were active at the time, yielded no positive fleas.     

Role of the Yersinia pestis yersiniabactin iron acquisition system in the incidence of flea-borne plague

Plague is a flea-borne zoonosis caused by the bacterium Yersinia pestis. Y. pestis mutants lacking the yersiniabactin (Ybt) siderophore-based iron transport system are avirulent when inoculated intradermally but fully virulent when inoculated intravenously in mice. Presumably, Ybt is required to provide sufficient iron at the peripheral injection site, suggesting that Ybt would be an essential virulence factor for flea-borne plague. Here, using a flea-to-mouse transmission model, we show that a Y. pestis strain lacking the Ybt system causes fatal plague at low incidence when transmitted by fleas. Bacteriology and histology analyses revealed that a Ybt-negative strain caused only primary septicemic plague and atypical bubonic plague instead of the typical bubonic form of disease. The results provide new evidence that primary septicemic plague is a distinct clinical entity and suggest that unusual forms of plague may be caused by atypical Y. pestis strains.     

Experimentally induced plague infection in the northern grasshopper mouse (Onychomys leucogaster) acquired by consumption of infected prey

In this study, 20 laboratory reared Onychomys leucogaster from a parental population that is naturally exposed to plague were each fed a white mouse that had been inoculated with Yersinia pestis. Three of the 20 O. leucogaster died, four survived with antibody titers against Y. pestis and 13 survived with no titer against Y. pestis. In contrast, when 20 O. leucogaster from a plague naive parental population were fed infected prey, seven died and 13 survived with no antibody titer against Y. pestis. Our results suggest another means by which O. leucogaster from populations that are naturally exposed to plague may acquire the disease.