2猪轮状病毒经细胞培养后对猪的感染试验

选用猪轮状病毒Na—86毒株,在MA104细胞上传至15、30、42、58、70、82及90代的细胞培养毒,口服感染未吮初乳的1日龄仔猪,观察其致病性的变化,结果证明,Na—86毒株在MA104细胞上传代繁殖后,随着代次的增加,对未吮初乳仔猪的致病力逐渐下降。15代次的细毒口服1毫升,足以使仔猪在37小时内发生腹泻。30～58代的细胞毒也能于3～36小时内使仔猪发生典型服泻。但70、72、82及90代毒,尽管每头接种量提高到10～15毫升,也不能引起仔猪腹泻,尤其82和90代细胞毒,重复回猪2～3次,结果一致。其90代细胞毒,在未吮初乳猪上连传3代,未见毒力反强,表明90代细胞毒是一株已失去致病性而较稳定的弱毒株,又在毒力反强试验中,从第1、2、3代回猪的肠内容物中,重新分离出90代细胞毒(核酸电泳证明病毒核酸型相同)。说明90代毒,虽未引起仔猪腹泻,但仍能在仔猪肠上皮细胞内生长繁殖。     

实验性水貂细小病毒性肠炎的病理形态学研究

健康水貂6只,3只作对照,另3只口服-20℃保存9个月的水貂细小病毒性肠炎粪毒。实验貂临床症状典型,小肠粘膜出现“气球样”上皮细胞,肠腺和绒毛上皮细胞广泛变性、坏死、脱落,胞浆内可见嗜酸性小体;胞核可见两种类型Cowdry A型包涵体;在肠系膜淋巴结、骨髓、脾和肾上腺也观察到了核内包涵体。在小肠绒毛上皮细胞膜上和肠腺腺腔中发现大量G-小杆菌。同时,用扫描电镜观察了各肠段粘膜表面的变化;用透射电镜研究了空肠前段粘膜上皮细胞中水貂细小病毒(MPV)的形态发生及其所引起的超微病变,发现核仁及其相随染色质参与了核内包涵体的形成。     

9株猪瘟分离毒株的致病特性

采用9株临床表现强、中、低致病特点的猪瘟野毒分离株第3代细胞毒作为种毒,按3mL/头剂量分别注射猪瘟抗原及抗体阴性猪,再用上一代传代猪发病后的血毒作为下一代接毒用种毒接种试验猪1头或2头,或上一代传代猪发病后,同圈放入1头或2头试验猪进行同居感染.如此进行,GDGZ1/95、BJCY1/96和JL1/94传至8代;FJFQ1/99传至7代;HeBHH1/95、HeNBY1/96、BJTX3/96、GXBH1/98和HeNXH2/98传至3代.结果显示:上述分离株传至3～5代过程中均表现出毒力增强的趋势,从3～5代传代到8(7)代的过程中毒力进一步增强并保持稳定,且均超过了标准石门强毒株的发病特点.所有试验猪均出现较典型的猪瘟临床症状,解剖后均表现出不同程度的病理变化,死后或解剖后的各种脏器经HCFA检查均为强阳性,这种现象进一步证实了猪是猪瘟病毒的敏感动物,各毒株之间毒力没有明显差异.对其中7株分离株传代血毒部分代次E2基因主要区域进行序列分析,结果仅GDGZ1/95株从F1～F8代中的F6代有2个核苷酸的差异,引起1个相应氨基酸的变异,其余毒株的不同代次没有碱基发生变异,初步说明猪瘟病毒基因型表现相对的稳定性.     

与王国威同志就《浅谈猪大肠杆菌病的病因及防治》一文商榷

贵刊今年第５期第２５页刊登王国威同志所著的 《浅谈猪大肠杆菌病的病因及防治》一文“对于患病仔 猪的治疗”项的第５条“患病仔猪出现腹泻脱水时,应 进行口服补液……”笔者对此有不同看法,现叙述如 下,请行家指教。 引起仔猪腹泻的大肠杆菌病临床上以仔猪黄痢 和仔猪白痢最为常见。 １．仔猪黄痢的发病机理：定植于仔猪小肠粘膜上 的致病菌产生一种蛋白外毒素,刺激隐窝部位肠粘膜 上皮细胞分泌大量液体,同时抑制绒毛上皮细胞的吸 收作用引起腹泻,导致脱水和代谢性酸碱平衡紊乱。 此时如果用口服法补液,则进入肠道内的液体因肠绒 …     

关于肠毒综合症问题

<正>肠毒综合症是一种由多病因引起的肠粘膜发炎、增厚、脱落、出血、坏死等变化的综合性病症。近些年来,本病发生比较普遍,特别是肉鸡的发生比     

产肠毒素性大肠杆菌主要毒力因子的研究进展

产肠毒素性大肠杆菌的毒力因子包 括黏附素,肠毒素,水肿病毒素,内毒素,溶血 素以及EatA。其中黏附素和肠毒素无论是 从发病学还是免疫学角度来讲,都扮演着很 重要的角色。猪源产肠毒素性大肠杆菌的黏 附素抗原主要有K88(F4),K99(F5),987P (F8)和F41,肠毒素包括耐热肠毒素与不耐 热肠毒素。     

家兔外伤性眼结膜炎的防治

<正> 发生本病的主要原因是灰尘或沙土吹入眼内,兔笼不清洁或有刺激性消毒药物(如氨水等)的刺激以及眼睑外伤等。外伤性结膜炎又分为卡他性结膜炎和化脓性结膜炎两种。病的初期表现为:流泪,怕光,眼睑粘膜潮红肿胀,眼睛半闭,眼睑和两颊皮肤由于流下的泪水经常刺激而发炎,从而引起绒毛脱落。如及时治疗,往往发展为化脓性结膜炎,同时引起眼睑粘膜严重充血,肿胀,眼睑变厚,尤其是边缘部分     

工感染雏鹅新型病毒性肠炎的病理形态学发展规律的研究

40只2日龄四川白鹅口服感染雏鹅新型病毒性肠炎病毒,在不同阶段解剖发病和死亡雏鹅,电镜观察组织器官的病理变化发展规律.接种后第2天,十二指肠绒毛顶部上皮细胞发生坏死、脱落.随着感染时间延长,上皮细胞的坏死、脱落迅速向绒毛基部发展,并伴随固有膜炎性细胞浸润和坏死,病变向着空肠段发展.进一步发展为纤维素性坏死性肠炎,于小肠中后段形成假膜包裹肠内容物的栓塞物或直接由纤维素性渗出物与坏死肠粘膜混合凝固形成栓塞物阻塞肠腔,使外观膨大.肺充血和出血.肾充血、出血及肾小管上皮细胞变性.部分病例肝颗粒变性、脂肪变性.后期部分病例气管、腺胃上皮细胞脱落.早期部分病例心充血和出血.食道、胰腺及脑正常.电镜下可观察到小肠上皮细胞核畸形、固缩、核仁消失、核膜模糊和胞核崩解;胞浆严重空化,形成含有很多病毒粒子的"封入体”;粗面内质网扩张呈囊状,其上的核蛋白体严重脱落;线粒体外膜破裂或嵴断裂及空化,部分受到损害的线粒体充满大量的病毒粒子;形成肠道栓子的外层假膜有大量的病毒粒子、细菌以及坏死的肠上皮细胞.肝脏细胞粗面内质网严重扩张及部分线粒体肿胀、脊断裂;而心肌细胞粗面内质网的轻度扩张及胞核畸形.本文还对雏鹅新型病毒性肠炎与小鹅瘟的病理变化进行了比较分析.     

防治鸡肠毒综合征的误区与经验

<正>肠毒综合征是一种由多病因引起的肠粘膜发炎、增厚、脱落、出血、坏死等变化的综合性病症,本病一年四季均能发生,但以夏、秋、冬季及气候和温差变化大的时候发生较多,任何日龄都能发生,特别是15～90日     

猪直肠脱出简易治疗

猪直肠脱出主要是由于大便秘结、顽固性下痢、母猪孕期便秘、冬天圈舍潮湿寒冷、猪体过瘦等原因引起的。其临床症状主要是直肠脱出肛门外 ,外表呈粗大的园柱状。初期肠粘膜充血呈红色 ,逐渐浮肿呈暗红色 ,表面干燥 ,并有出血点和龟裂 ,排粪十分困难 ,病猪不断努责 ,坏死的直肠也不断增长 ,导致肠穿孔引起大量流血而死亡。现将其简易治疗方法介绍如下。( 1 )初期直肠脱出 ,肠粘膜微充血 ,浮肿不明显 ,用 1 %高锰酸钾溶液清洗后把脱出的直肠慢慢送回腹腔内 ,在肛门周围注射75%酒精 1 0ｍｌ以防再脱。( 2 )脱出的直肠严重水肿 ,干燥龟裂 ,必须…     

猪轮状病毒弱毒苗免疫研究

用猪源轮状病毒弱毒株－Ｎａ８６Ｆ９０制成的疫苗先后免疫母猪２５０头，乳中抗ＲＶ的ＩｇＡ最高滴度为８１９２０，对照组最高滴度仅有１６０；产后１个月，免疫组滴度仍维持在５１２０以上，而对照组仅４０；免疫组仔猪哺乳期轮状病毒检出率下降３７．２％，断奶仔猪育成率由７５％提高到９０％以上，断奶后窝重由平均１３０～１５０ｋｇ，提高到２００～２５０ｋｇ     

CHANGES IN INTESTINAL STRUCTURE AND FUNCTION OF NEONATAL CALVES INFECTED WITH REOVIRUS-LIKE AGENT AND ESCHERICIA COLI

Measurements of villus/crypt length ratio and mucosal beta-galactosidase activity were made on calves less than 3 weeks of age which had diarrhoea associated with reovirus-like agent and E. coli. In calves with diarrhoea, the villus/crypt length ratios at all sites examined along the small intestine were less than in normal calves of similar age. This was attributed to a reduction in length of vili in calves infected with the reovirus-like agent. The activity of mucosal beta-galactosidase in the intestine of calves with diarrhoea was less than in normal calves, at all sites examined. A relationship existed between beta-galactosidase activity in vitro and lactose hydrolysis in vivo. It was concluded that calves with diarrhoea associated with reovirus-like agent, have a reduced ability to utilize dietary lactose.     

Comparative virulence of two porcine group-A rotavirus isolates in gnotobiotic pigs

The virulence of 2 porcine group-A rotavirus isolates was compared. Forty hysterotomy-derived 3-day-old gnotobiotic pigs were inoculated orally with 2 ml of intestinal homogenate containing either the Ohio State University (OSU) or the South Dakota State University (SDSU) strain of porcine rotavirus or were inoculated with medium only. Clinical signs of disease, body weight, distribution of viral antigen, fecal excretion of virus, and histologic lesions (observed by light and scanning electron microscopy) were determined. Morphometric measurements of villi and crypts were made. In pigs inoculated with OSU or SDSU strains, diarrhea began at postinoculation hours (PIH) 19 to 48 and PIH 24 to 54, respectively. None of the virus-infected pigs died as a consequence of infection and all had similar clinical signs of disease, body weight changes, and virus-shedding patterns, regardless of the strain of rotavirus with which they were infected. Microscopic findings in the small intestine of virus-infected pigs were similar, except that the SDSU strain caused more severe villus atrophy and villus fusion in the duodenum at PIH 72 and 168 than was associated with the OSU strain. Viral antigen in the small intestine of pigs infected with either virus was observed by use of immunofluorescence at PIH 24 and 72, but was seldom seen at PIH 168.     

Experimental infection and cross protection tests in calves with cytopathic strains of bovine rotavirus

Four cytopathic strains (81/32F, 81/36F, 81/40F, 82/80F) of bovine rotavirus were shown to be pathogenic for conventionally reared newborn calves. Calves were infected orally, using 3 calves for each isolate. All became febrile, were depressed and diarrhoeic. Two calves, one of which in the group of those infected with 81/36F isolate, and the other infected with strain 81/40F, were killed when moribund. A 3rd calf from the 81/36F infected group, died. At necropsy localized lesions of the small intestines, which are considered to be typical of rotavirus infection, were found. Virus was consistently isolated from the fecal samples of the inoculated calves up to 13 days post-inoculation. It was speculated that some differences existed in the virulence of the bovine rotaviruses tested. The cross protection tests revealed that 1 strain (81/36F) might be antigenically more complex than the others.     

Detection of rotavirus in experimentally infected piglets.

Scouring and vomiting was induced in piglets by experimental infection with a field strain of rotavirus. Virus or viral antigen was detected in the small intestine by the fluorescent antibody technique and virus could also be demonstrated in infected tissue culture cells by immuno-fluorescence. Progeny particles in the epithelial layer of the small intestine were identified by electron microscopy. Three morphological types could be distinguished, often associated with electron-dense inclusion, and infected cells, though small in number, were present throughout the length of the small intestine.     

Quantitative observations on experimental reo-like virus (rotavirus) infection in colostrum-deprived calves.

Ten calves were challenged with one of two strains of reo-like virus (rotavirus). Changes in the daily faecal and urinary outputs were monitored and packed cell volume, plasma sodium, potassium and urea levels were measured. Faeces were examined for the presence of rotavirus by direct electron microscopy and immunofluorescence in cultures of PK(15) cells. All calves excreted rotavirus in the faeces for several days. Two calves remained clinically normal throughout the experiment, but in the remaining calves, faeces became mucoid in consistency and yellow-white in colour. In only two calves did the daily faecal output exceed 500 g with a fall in the dry matter content to less than 10 per cent. Slightly elevated blood urea levels and hyperkalaemia were the only changes observed in blood chemistry and these quickly returned to normal. Virus antigen was observed in the epithelial cells by immunofluorescence in the proximal and middle small intestine of calves. Pathological lesions occurred predominantly in the proximal small intestine of nine calves examined.     

Pathological changes in the small intestine of neonatal calves naturally infected with reo-like virus (rotavirus).

Nine calves, of which six had been challenged with an enteropathogenic strain of Escherichia coli, were found to be naturally infected with rotavirus. Rotavirus was recovered from the faeces of six calves and rotavirus antigen was detected in the intestinal mucosa of all calves. Stunting and fusion of villi were seen principally in the proximal and middle small intestine, where rotavirus antigen was detected by immunofluorescence. Typical lesions of enteric colibacillosis were found in the distal ileum of the challenged calves, associated with adhesion of the challenge strain of E coli to the mucosa. All samples were removed from the intestine under general anaesthesia and denudation of villi was not observed. However, following exsanguination and resampling at the same site in the small intestine of one calf, denudation was a constant feature.     

Rotavirus replication in colostrum-fed and colostrum-deprived pigs

A porcine rotavirus isolate was titrated in neonatal colostrum-fed and colostrum-deprived pigs. The stock rotavirus suspension had a titer of 10(-6.5)/ml and was in its fifteenth cell culture passage in MA-104 cells. Fourteen colostrum-fed pigs were orally inoculated with dilutions of the stock virus suspension ranging from undiluted to 10(-5). These pigs did not develop notable clinical signs during the 7-day experimental trial and no pathologic changes were found in intestine, liver, lung, kidney, spleen, or brain. However, rotavirus was detected in feces of the colostrum-fed pigs, using virus isolation and electron microscopic techniques. Rotavirus was also isolated from lung, brain, or spleen of 4 of 12 of these pigs. Sixteen colostrum-deprived pigs were orally inoculated with dilutions of the stock virus suspension ranging from 10(-1) to 10(-8). Diarrhea developed in 10 of 12 pigs that were given up to the 10(-6) dilution. Seven of these 12 pigs died because of the severity of diarrhea. Pigs that died of rotavirus-induced diarrhea had severe villus loss in the jejunum and ileum. Villi of the small intestine of colostrum-deprived pigs that survived the severe diarrhea were within normal limits at the end of the 7-day trial. The colostrum-deprived pigs that were inoculated with a dilution less than 10(-6) and survived past 96 hours underwent seroconversion. Rotavirus was detected by virus isolation and electron microscopy in the feces of all colostrum-deprived pigs that survived beyond 18.5 hours after inoculation. Virus was isolated from lungs, brain, or spleen of 12 of 16 colostrum-deprived pigs.     

A study of the basis of virulence variation of bovine rotaviruses.

Rotaviruses are enteric pathogens of cattle but sub-clinical infections are common. Virulence variation has been identified with bovine rotaviruses and some rotaviruses replicated without clinical signs in non-immune calves. The rotavirus genome is composed of eleven segments of double-stranded RNA and the fourth largest segment codes for a non-glycosylated surface protein, VP4, which has been linked with virulence. In the present study the biological basis of rotavirus virulence variation was studied in vivo and compared with the known properties of the fourth gene. Calves were inoculated orally with a virulent rotavirus or a rotavirus of low virulence which multiplied but failed to cause diarrhoea. They were taken for necropsy at intervals of 2 days after inoculation. Clinical signs, virus in faeces and the percentage of infected small intestinal epithelium were determined. Damage to the small intestine was assessed by measurement of villus heights and crypt-cell production rates. Virulence was associated with a greater level of colonization of the small intestinal epithelium, greater enterocyte damage and preferential infection of the upper small intestine. The fourth gene determines the ability of rotaviruses to spread in vitro and the finding that virulence was associated with greater colonization in vivo raises the possibility that this gene may have an important role in rotavirus virulence.     

Pathology of natural rotavirus infection in clinically normal calves

During a longitudinal study of the epidemiology of rotavirus infection in a calf rearing unit, excretion of virus in faeces was detected by enzyme-linked immunosorbent assay in 40 of 48 (83 per cent) unweaned calves aged between three days and five weeks. Fifty per cent of the infected calves had no clinical signs of disease. Enterocytes containing rotavirus antigen and intestinal lesions were found in all of 12 clinically normal calves selected for necropsy between days 1 and 4 of virus excretion. Stunting and fusion of villi, exfoliation, disarrangement and vacuolation of enterocytes and the presence of cuboidal enterocytes were observed in infected calves but not in rotavirus-free control calves. Lesions predominated in the upper small intestine, where rotavirus was most abundant, especially on the first two days of virus excretion. The numbers of enterocytes infected with rotavirus diminished before the lesions resolved.