贵州省部分大型水电建设工程地区鼠疫疫源调查结果分析

目的调查贵州省水电开发地区的鼠疫疫源状况,为制定鼠疫预防控制措施提供依据。方法运用现场流行病学方法调查7个大型水电站建设工程地区的18个县(市)的54个涉淹乡镇,采集啮齿动物、蚤类、指示动物和正常人血标本,检测鼠疫菌、鼠疫FI抗原和FI抗体。结果从天生桥电站库区调查标本中检出鼠疫FI抗原阳性21份、FI抗体阳性14份,分离到鼠疫菌3株。其他水电站库区调查标本未检出鼠疫阳性指标。结论天生桥水电站库区为已确定的黄胸鼠鼠疫疫源地。龙滩、平班和光照三个水电站库区调查结果虽然没有检获鼠疫感染阳性指标,但是具有形成黄胸鼠鼠疫疫源地的基本条件。洪家渡、引子渡和三板溪电站库区的调查资料表明该地区不具备形成黄胸鼠鼠疫疫源地的基本条件。但由于工程建设的原因,这些地区的自然生态环境必然有所改变,因此十分有必要加强这些工程地区的鼠疫监测和库区蓄水前的大面积灭鼠工作。     

西北地区喜马拉雅旱獭鼠疫自然疫源地鼠疫流行特点及控制

近年来，我国西北地区喜马拉雅旱獭鼠疫自然疫源地进入相对活跃期，人间鼠疫几乎每年都有发生。本文主要介绍了该地区鼠疫流行病学特点，并提出相应控制措施。     

梁河家鼠鼠疫疫源地鼠疫噬菌体的分离及其流行病学意义

目的 调查梁河县家鼠鼠疫疫源地宿主动物中是否携带鼠疫噬菌体,并探讨其流行病学意义。方法 2017年采集梁河家鼠鼠疫疫源地4个曾流行过鼠疫乡镇的鼠类标本,以鼠疫疫苗株EV76为饲养菌,采用双层平板法分离鼠疫噬菌体,同时挑取部分噬菌体进行电镜扫描。结果 共获得338份标本(黄胸鼠234只,臭鼩鼱43只,其余61只),分离到29株鼠疫噬菌体,总分离率为8.58%(29/338),其中19株分离自黄胸鼠,分离率为8.12%(19/234),8株分离自臭鼩鼱,分离率为18.6%(8/43);4个乡镇全部有分离到鼠疫噬菌体,其中遮岛镇分离率最高为16.13%(5/31);初次分离这些鼠疫噬菌体时,其噬斑在双层平板上表现为大(直径≥2.0 mm)、中(≥1.0 mm,≤2.0 mm)及小(≤1.0 mm)3种噬斑;2株有代表性噬菌体皆为肌尾病毒科噬菌体。结论 梁河家鼠鼠疫疫源地中普遍存在鼠疫噬菌体,黄胸鼠是主要的携带宿主,所分鼠疫噬菌体为肌尾病毒科噬菌体且具有多态性,值得进一步研究。     

An update on clinical immunology,immune mechanisms and deficiency diseases

29th Annual Jackson Hole, Wyoming, Update in Clinical Immunology, Microbiology and Infectious Diseases

Salt Lake city, UT, USA, 9–13 July 2012

The 29th Annual Jackson Hole, Wyoming, Update in Clinical Immunology, Microbiology and Infectious Diseases was held from 9 to 13 July 2012. This postgraduate, continuing medical education course of the University of Utah’s Department of Pathology (UT, USA) is designed for laboratorians, clinical pathologists, pathologists, clinicians, clinical immunology and infectious disease specialists and medical technologists, as well as residents and fellows training in immunology, microbiology or infectious diseases.     

剑川野鼠鼠疫疫源地鼠疫噬菌体的分离及其流行病学意义

目的 调查剑川野鼠鼠疫疫源地宿主动物中是否携带鼠疫噬菌体,并探讨其流行病学意义。方法 2017年1-6月采集剑川野鼠鼠疫疫源地4个曾流行过鼠疫乡镇6个自然村的鼠类标本,以鼠疫疫苗株EV76为饲养菌,采用双层平板法分离鼠疫噬菌体,并对分离结果进行流行病学分析,同时挑取部分噬菌体进行电镜扫描。结果 共获得641份标本（齐氏姬鼠334只,大绒鼠236只,其余71只）,分离到9株鼠疫噬菌体,总分离率1.40%;有4个疫点（白山母村、石龙村、新松村、大庆村）分离到了鼠疫噬菌体,另外2个点（长乐村、西门社区）未分到鼠疫噬菌体;9株鼠疫噬菌体中,8株分离自齐氏姬鼠,1株自大绒鼠;初次分离这些鼠疫噬菌体时,其噬斑在双层平板上表现为大（直径~2.0 mm）、中（~1.0 mm）及小（<0.5 mm）3种噬斑;4株有代表性噬菌体皆为肌尾病毒科噬菌体。结论 剑川野鼠鼠疫疫源地中普遍存在鼠疫噬菌体,齐氏姬鼠是主要的携带宿主,所分鼠疫噬菌体为肌尾病毒科噬菌体且具有多态性,值得进一步研究。     

达乌尔黄鼠及其寄生蚤的杀灭研究

目的为了更好地控制鼠疫流行,筛选出安全、高效、使用方便的灭蚤药物。方法堵洞查盗法、探洞干蚤法。结果磷化铝灭蚤效果最好,可以达到鼠蚤并灭的目的。而灭鼠烟雾剂有一定的灭蚤效果。0.005%溴敌隆毒饵不能够杀灭鼠类的寄生蚤。结论磷化铝作为熏蒸杀虫剂,一旦发生动物间鼠疫,在鼠疫疫区大面积灭鼠灭蚤时推广使用。     

From the Cover: Silencing urease: A key evolutionary step that facilitated the adaptation of Yersinia pestis to the flea-borne transmission route

The arthropod-borne transmission route of Yersinia pestis, the bacterial agent of plague, is a recent evolutionary adaptation. Yersinia pseudotuberculosis, the closely related food-and water-borne enteric species from which Y. pestis diverged less than 6,400 y ago, exhibits significant oral toxicity to the flea vectors of plague, whereas Y. pestis does not. In this study, we identify the Yersinia urease enzyme as the responsible oral toxin. All Y. pestis strains, including those phylogenetically closest to the Y. pseudotuberculosis progenitor, contain a mutated ureD allele that eliminated urease activity. Restoration of a functional ureD was sufficient to make Y. pestis orally toxic to fleas. Conversely, deletion of the urease operon in Y. pseudotuberculosis rendered it nontoxic. Enzymatic activity was required for toxicity. Because urease-related mortality eliminates 30–40% of infective flea vectors, ureD mutation early in the evolution of Y. pestis was likely subject to strong positive selection because it significantly increased transmission potential.Among the 18 species that compose the genus Yersinia three are pathogenic for humans: Yersinia pestis, the causative agent of plague, and the enteric pathogens Yersinia pseudotuberculosis and Yersinia enterocolitica. Whereas Y. enterocolitica and Y. pseudotuberculosis diverged between 41 and 186 Ma, comparative genomics and population genetic studies indicate that Y. pestis has evolved from Y. pseudotuberculosis only within the last 1,500–6,400 y (1–4). Thus, the two species share most of their genome repertoire but despite this close genetic relationship they cause very different diseases and have very distinct transmission routes. Y. pestis causes acute and often fatal bubonic, septicemic, and pneumonic forms of plague and is transmitted primarily by flea bites (5). In contrast, Y. pseudotuberculosis causes relatively mild food- and water-borne diseases and is transmitted by the fecal–oral route (6).The recent evolution of flea-borne transmission of Y. pestis has involved sequential gene loss and acquisition steps (7). Y. pestis has acquired two unique plasmids that are not present in Y. pseudotuberculosis: pMT1, required for colonization and bacterial survival in the flea midgut (8), and pPCP1, which is irrelevant to the bacteria–flea interaction but which facilitates bacterial dissemination from the flea bite site (9–11). The major transmission mechanism of Y. pestis depends on its ability to grow as a biofilm in the flea proventriculus, a muscular valve in the flea foregut that connects the esophagus to the midgut (12). The blockage impedes fleas from taking a full blood meal, resulting in repeated feeding attempts, during which some of the bacteria are dislodged from the biofilm and transmitted into the host (12, 13). Selective loss of gene function has been important to the development and stability of Y. pestis biofilm in the flea required for full transmissibility (7, 14, 15).Studies on the interaction of Y. pseudotuberculosis with fleas revealed another important adaptive change in the evolution of Y. pestis into a flea-borne pathogen. Y. pseudotuberculosis is orally toxic to Xenopsylla cheopis fleas, an important plague vector species. Shortly after taking a blood meal containing Y. pseudotuberculosis, about one-third to one-half of fleas show signs of acute toxicity, including diarrhea and immobility, leading to the death of up to 40% of the infected fleas (16). However, very little is known about the Y. pseudotuberculosis factor(s) responsible for toxicity to fleas; it has been characterized only as a nonsecreted protein specifically active in the flea digestive tract, the production of which is not regulated by temperature—toxicity occurs whether the bacteria are grown at 21 °C or 37 °C (16). The Yersinia toxin complex (Tc) insecticidal-like proteins have been ruled out as the cause of oral toxicity to fleas (16).In this study, we used comparative proteomics, functional genetics, and biochemical approaches in conjunction with a flea infection model to identify the Yersinia urease enzyme as the flea-toxic factor. Phylogenetics analyses indicate that functional urease activity was lost early in the divergence of Y. pestis and epidemiologic modeling suggests that this gene loss was subject to strong positive selection because it significantly increased transmission probability.     

云南省2018年动物间鼠疫监测调查与分析

目的 掌握和分析云南省2018年鼠疫疫情现况,为鼠疫防控对策提供科学依据。方法 2018年对云南省104个县(市)开展鼠疫宿主、媒介、病原学和血清学监测,并对监测结果统计学分析。结果 黄胸鼠疫源地以黄胸鼠、褐家鼠为优势种;齐氏姬鼠-大绒鼠疫源地以齐氏姬鼠、大绒鼠为优势种,黄胸鼠疫源地黄胸鼠鼠体蚤以印鼠客蚤和缓慢细蚤为主;褐家鼠以缓慢细蚤、人蚤和印鼠客蚤为主。齐氏姬鼠-大绒鼠疫源地齐氏姬鼠鼠体蚤以棕形额蚤、特新蚤指名亚种为主;大绒鼠鼠体蚤以方叶栉眼蚤为主,特新蚤指名亚种为次要寄生染蚤种。对47 618只动物进行细菌学检验,检出鼠疫菌4株;对20 710组媒介进行细菌学检验,结果均为阴性。应用鼠疫间接血凝试验方法检验动物血清20 105份,阳性4份,应用鼠疫反相间接血凝试验方法检验动物脏器23份,阳性5份。结论 云南省野鼠疫源地玉龙县和古城区发生动物鼠疫流行,流行强度猛烈,家鼠疫源地未发生鼠疫疫情,但是形势不容乐观,应加强对全省鼠疫的监测和健康教育工作。