猪口蹄疫与传染性水泡病的异同

<正>1口蹄疫口蹄疫是由口蹄疫病毒引起偶蹄动物的一种急性、热性、高度接触性的传染病。1.1猪口蹄疫的病状是口腔粘膜和蹄部的皮肤形成水     

猪水泡病的诊断与防治

猪水泡病是由猪水泡病毒引起的急性、热性、接触性传染病。其特征是流行性强、发病率高,蹄部、口腔、鼻端、腹部及乳头周围皮肤和黏膜发生水泡或烂斑。     

菌毒净对猪O型口蹄疫病毒和猪水泡病病毒的杀灭效果

用试管中和灭毒,实验动物验证的方法测定菌毒净消毒剂对猪Ｏ型口蹄病毒和猪水泡病病毒的杀灭效果。试验结果表明,１：１００００的菌毒净消毒剂可完全杀灭猪Ｏ型口蹄疫病毒,１：８０００的菌毒净可完全杀灭猪水泡病病毒。     

应用IIF筛选抗口蹄疫和抗猪水泡病病毒单抗的研究

应用间接免疫荧光方法（ⅡＦ）进行筛选，获得３株稳定分泌特异性抗口蹄疫病毒（ＦＭＤＶ）单抗的杂交瘤细胞的２株稳定分泌特异性抗猪水泡病毒（ＳＶＤＶ）单抗的杂交瘤细胞。ＩＩＦ重复测试阳性和阴性杂交瘤细胞上清，结果完全相符。ＩＩＦ特异性试验表明，３株抗ＦＭＤＶ单抗只与ＦＭＤＶ反应，而不与相关的ＳＶＤＶ和ＰＤ１５细胞反应，反之２株抗ＳＶＤＶ单抗只与ＳＶＤＶ反应，而不与ＦＭＤＶ和ＰＤ１５细胞反应。实验证明，Ｉ     

猪口蹄疫和水泡病病毒免疫鉴别诊断方法的比较研究

通过单克隆抗体斑点酶联免疫吸附试验（ＭｃＡｂＤｏｔＥＬＩＳＡ）和反向间接血凝试验（ＲＩＨＡ）分别对猪口蹄疫病毒（ＦＭＤＶ）和水泡病病毒（ＳＶＤＶ）检测比较。试验表明,ＭｃＡｂＤｏｔＥＬＩＳＡ特异性强,快速简便,比ＲＩＨＡ更为敏感、稳定、直观。本研究在猪口蹄疫和水泡病单抗联合诊断药盒的研制方面是一个有益的尝试。     

多重RT-PCR检测猪口蹄疫病毒、猪水泡病病毒和猪水疱性口炎病毒的研究

建立了一种同时检测猪口蹄疫病毒(FMDV)、猪水泡病病毒(SVDV)和猪水疱性口炎病毒(VSV)三种病原体的多重RT-PCR方法。参照文献报道的基因序列,设计合成了三对特异性引物;PCR扩增条件进行优化后,用这三对引物对同一样品中的FMDV、SVDV、VSVRNA模板进行扩增,结果同时得到了三条特异性条带,大小与试验设计相符:FMDV(208bp)、SVDV(862bp)、VSV(638bp),且对猪瘟病毒(CSFV)、猪繁殖与呼吸综合症病毒(PRRSV)和猪传染性胃肠炎病毒(TGEV)核酸扩增结果为阴性;三种病毒RNA模板检出的最小量均为10fg。试验证明,此方法经济、快速、敏感、特异,可用于FMDV、SVDV和VSV这三种猪水泡性疾病的鉴别诊断及流行病学调查。     

猪水泡病的诊断与防治

猪传染性水疱病又称猪水疱病（swine vesicular disease,SVD）,是由猪水疱病病毒引起的一种急性、热性、接触性传染病。以猪鼻端、口腔黏膜、蹄冠、趾间、蹄踵和乳房部皮肤出现水疱为特征,该病具有很强的传染性,发病率较高,自然情况下仅有猪发病,其他家畜均不发病,各种年龄、品种、性别的猪均易感。     

猪瘟病毒分子生物学研究进展

猪瘟病毒 (CSFV)是一种具有囊膜的 RNA病毒 ,在病毒分类上属于黄病毒科、瘟病毒属的成员 ,也是世界上危害最严重的猪的病原之一 ,被国际兽医局 (OIE)列为 A类动物传染病 ,因此开展猪瘟病毒分子生物学研究具有重要的经济意义。1　CSFV基因组结构和功能CSFV基因组为单股正链 RNA,长约 1 2 .3 kb,含有一个大的开放阅读框架 ,并由其编码一种约3 898个氨基酸的多聚蛋白 ,该聚蛋白在翻译的同时和翻译后经病毒和宿主细胞的蛋白酶加工成 1 2种成熟的病毒蛋白 ,其在聚蛋白上从 N端到 C端的顺序依次为 :Npro、C、Ems、E1、E2、p7、NS2、N…     

Physico-chemical properties of swine vesicular disease virus]

Titration of SVDV on primary pig kidney cell cultures revealed a plating efficiency of less than or equal to 0,9 X 10(-3). Concentration and purification of the SVD-Virus propagated on pig kidney cell cultures were done by chloroform treatment, adsorption, differential- and density gradient centrifugation. The following physical parameters were found: SVDV is an isometrical RNA-virus having a diameter of 25,1 +/- 1,0 nm. It is resistent to the action of chloroform, ether and pH. The virus has a sedimentation coefficient of 156 +/- 3S and a bouyant density in CsCl of 1,33 +/- 0,01 g/ml. Within the family of picornaviruses the SVDV belongs to the subgroup of enteroviruses and can be distinguished from the foot-and-mouth disease virus by the difference in pH-sensitivity and bouyant density in CsCl.     

Pathogenesis of swine vesicular disease in pigs.

Pigs exposed to swine vesicular disease virus developed vesicular lesions by postinoculation day 2. Lesions first appeared on the coronary band and then on the dewclaw, tongue, snout, lips, and bulbs of the heels. The onset of viremia coincided with febrile response and the appearance of vesicles. Virus was isolated from the nasal discharge, esophageal-pharyngeal fluid, and feces as early as postinoculation day 1. Greater amounts of virus were isolated from samples collected during the first week of infection, and lesser amounts from samples collected during the second week. The appearance and the distribution of specific fluorescence in various tissues indicated that during the development of swine vesicular disease virus infection, the epithelial tissues were initially involved, followed by a generalized infection of lymph tissues, and subsequently, a primary viremia. Seroconversion was detectable as early as postinoculation day 4. A mild nonsuppurative meningoencephalomyelitis throughout the CNS was observed in both inoculated and contact-exposed pigs. The olfactory bulbs were most severely and were frequently affected, particularly in contact pigs. The most severe brain lesions were found in pigs 3 to 4 days after the onset of viremia; contact pigs showed more severe brain lesions than inoculated pigs. Microscopic changes were also found in the coronary band, snout, tongue, and heart.     

Experimental swine vesicular disease, pathology and immunofluorescence studies.

Two day old piglets were inoculated intravenously with 1 ml of swine vesicular disease virus UK-G 27-72 isolate. Using infectivity tests, immunofluorescent staining and gross and histopathological examination, pathogenesis of the infection was studied in tissue specimens collected daily from one through seven days postinoculation. Swine vesicular disease virus had a strong affinity for the epithelia of the tongue, snout, coronary band and lips, the myocardium and the lymphoid elements of the tonsil and the brain stem. The virus had the greatest affinity for the epithelium of the tongue. However, there was no evidence that the tongue was the initial replication site for swine vesicular disease virus. Prickle cells in the stratum spinosum appear to be the primary targets for the virus. The necrotic foci in the stratum spinosum appeared first, followed the next day by reticular degeneration and multilocular intraepidermal vesicular formation. In the digestive tract and most of the other visceral organs the short duration and sudden drop of the virus titres and the negative fluorescence and pathological findings suggest that these are not important sites for the replication of swine vesicular disease virus in this experiment. The virus was recovered from most of the central nervous tissue specimens. Although the piglets had significant central nervous system lesions, signs of impaired central nervous system function were not detected. However, subtle nervous signs could have been obscured by difficulties in locomotion resulting from severe lesions of the feet.