口蹄疫的流行与防制

口蹄疫(FMD)是一种危害严重的偶蹄动物传染病,本文从流行病学、临床病理变化以及消毒技术、治疗措施和疫病控制等方面对口蹄疫的流行与防制的研究作以综述.     

福建南部养殖石斑鱼暴发性疾病流行调查

近年来福建南部网箱养殖石斑鱼常暴发急性传染病,经试验确认的传染病病原有神经坏死病毒、微孢子虫、本尼登虫以及多种弧菌.由神经坏死病毒引起的病毒性神经坏死病表现典型的神经症状,中枢神经组织和视网膜细胞严重空泡坏死;微孢子虫病表现为腹部、生殖腺、肝脏、肌肉等组织寄生大量孢子囊;本尼登虫主要寄生于石斑鱼的体表;感染的细菌主要有溶藻弧菌、副溶血弧菌以及河流弧菌等10种,这些菌多为条件致病菌.调查结果表明,病毒性神经坏死病是该地区养殖石斑鱼最常见危害也最大的传染病.     

河南省猪瘟流行现状调查及净化措施研究

对25个猪场191头疑似猪瘟病猪进行流行病学调查,病理剖检,兔体接种试验及反转录多聚酶链反应(RT-PCR)检测,发现仔猪猪瘟阳性检出率平均为77.4%,并呈快速上升趋势。RT-PCR法检测猪瘟快速、准确。调查显示我省猪瘟流行和发病出现一些新的特点,疫情呈蔓延和增加的趋势。对5个猪瘟污染猪场实行定期检测,淘汰带毒猪,培育健康无猪瘟带毒的种猪群和后备种猪群为主,制定合理的免疫程序,采取同步防治其他疾病的猪瘟综合防治措施,取得了很好的效果。     

甘肃省马肿瘤的流行病学调查

采用流行病学方法,1991～2003年对甘肃省各地州市的各个牧场和分散饲养马的肿瘤的发病情况进行了调查,并采用病理解剖学和组织学方法对病例进行确诊,结果表明:在甘肃省马肿瘤中良性肿瘤的发病率明显高于恶性肿瘤,其中发病最多的为纤维瘤,占全部肿瘤的42.31%,且公马的纤维瘤发病率比母马高;调查还发现马肿瘤的发病率与年龄有关,多发于5～10岁;同时还发现马肿瘤的高发区与人肿瘤的高发区地域分布一致。     

广西规模猪场主要疫病的流行病学调查与防治

结合流行病学、临床症状、病理变化,采用PCR技术,对2005年1~6月间广西36个发生疫病的规模猪场提供的肝、脾、淋巴结、脑等84份组织病料进行猪繁殖与呼吸综合症(PRRS)、猪瘟(CSFV)、猪伪狂犬病(PRV)、猪圆环病毒2型(PCV-2)检测。结果,检出PRRS阳性病料37份,阳性率44%,阳性场17个,场阳性率47%;CSFV阳性病料16份,阳性率11.9%,阳性场6个,场阳性率22.2%;PRV阳性病料27份,阳性率32.1%,阳性场12个,场阳性率33.3%;PCV-2阳性病料44份,阳性率52.3%,阳性场21个,场阳性率58.3%。同时还发现组织病料和发病猪场中存在猪繁殖与呼吸综合症、猪瘟、猪伪狂犬病、猪圆环病毒2型不同程度的混合感染现象,其中PRRS、PCV-2混合感染最为严重,样品阳性率33.3%,场阳性率25%。表明广西规模猪场主要疫病十分复杂,混合感染现象比较普遍,对广西养猪业带来巨大威胁,应加强疫病的防控工作。     

河南猪隐孢子虫病流行病学调查及动物感染试验

为了掌握河南猪隐孢子虫(Cryptosporidium)的感染情况,用饱和糖溶液漂浮法和改良抗酸染色法调查了郑州、许昌、漯河和禹州等地市6个猪场共417份粪样,并进行了固始品种雏鸡和昆明系小白鼠和长大二元杂交仔猪的动物感染试验.结果表明,根据形态大小初步鉴定为小球隐孢子虫(Cryptosporidium parvum),平均感染率为10.95%,20日龄以前的仔猪未感染,21~40日龄的的仔猪感染率为12.20%,41~60日龄的仔猪感染率为21.19%;猪源隐孢子虫分离株(sucp)不感染5日龄固始品种雏鸡和18日龄正常的昆明系小白鼠,但是能感染免疫抑制小白鼠,对4日龄仔猪有较强的致病性,并且出现严重的拉稀、脱水等症状.组织切片用H.E染色观察结果显示,sucp株寄生在小白鼠的十二指肠、空肠和回肠以及仔猪的盲肠、结肠和直肠.     

一个种猪场猪伪狂犬病疫情四年追踪调查报告

对某中型集约化种猪场４年继发猪伪狂犬病疫情进行了追踪调查。疫病流行于带仔母猪舍，主要是７￣１２日龄仔猪发病，１９９４年暴发流行时，窝发病率为４３．７％，发病窝仔猪发病率为８６．７％，病死率为９３％。疫情平息后，对全场经产母猪接种过伪狂犬病疫苗。１９９５￣１９９７年在带仔母猪舍又继发流行，窝发病率分别为３２％，３４％和２９％，其发病窝仔猪发病率和病死率较首发时低。     

Spatial estimation of the density and carbon content of host populations for Phytophthora ramorum in California and Oregon

Outbreak of the emerging infectious disease sudden oak death continues to threaten California and Oregon forests following introduction of the exotic plant pathogen Phytophthora ramorum. Identifying areas at risk and forecasting changes in forest carbon following disease outbreak requires an understanding of the geographical distribution of host populations, which is unknown. In this study, we quantify and map the population density and carbon contents of five key host species for P. ramorum in California and Oregon, including four hosts killed by the pathogen (Notholithocarpus densiflorus, Quercus agrifolia, Quercus kelloggii and Quercus chrysolepis) and the foliar host Umbellularia californica which supports high sporulation rates. We integrate multiple sources of vegetation data, assembled from sparsely distributed (regional-scale) forest inventory and analysis (FIA) plots and more densely distributed (landscape-scale) plots for monitoring sudden oak death, and develop spatial prediction models based on correlation with environmental variables and spatial dependencies in host abundance. We estimate that 1.8 billion N. densiflorus trees (68 Tg C) and 2.6 billion Quercus host trees (227 Tg C) occur across 3.9 and 17.7 million ha of their respective habitat. A total of 436 million U.californica trees (14 Tg C) occur across 4.2 million ha which frequently overlap with Quercus and N. densiflorus host populations. Combination of landscape-scale data with FIA data resulted in more accurate estimation of host populations and their carbon contents. Forests of northern California and southwest Oregon have the highest concentration of the most susceptible hosts along with climatic conditions that favor pathogen spread. This study represents the first spatially-explicit estimate of P. ramorum host populations and their carbon contents which exceed previously published estimates. Our results will inform landscape- to regional-scale models of disease dynamics and guide management decisions regarding ecosystem impacts including risk of C release following widespread tree mortality.     

Characterization of monilia disease caused by Monilinia linhartiana on quince in southern Spain

This study elucidates the aetiology and epidemiology of monilia disease of quince caused by the fungus Monilinia linhartiana in Spain. Disease incidence and the dynamics of apothecial development and ascospore discharge were quantified and the pathogen was characterized using morphological and molecular methods. The pathogen did not produce conidia or apothecia on agar media but produced conidia on leaves showing symptoms and apothecia on mummified young quince fruit. Monilinia linhartiana was not pathogenic on ripe quince fruit but was readily isolated from developing, mummified fruit (pseudosclerotia). Phylogenetic analysis based on 5·8S‐ITS region sequences placed M. linhartiana in the Disjuntoriae section of Monilinia species infecting rosaceous hosts. Studies during 2004–2008 in four commercial orchards in southern Spain determined two major infection periods for the disease. The first coincided with the unfolding of the first leaves and resulted in leaf blotch and shoot blight. The second coincided with flowering and led to mummification of developing young fruit. Foliar infection was apparently initiated by airborne ascospores produced on pseudosclerotia that overwintered on the soil surface, while flower infection was probably initiated by conidia produced on leaf lesions. Incidence of diseased shoots ranged from 1 to 91% and was correlated with calculated inoculum potential, based on the density and maturity of apothecia formed on pseudosclerotia. This epidemiological study has made it possible to characterize the life cycle of monilia disease on quince in southern Spain, which will help the development of new control strategies.