犬细小病毒病的病理学观察

对2例萨摩耶犬的犬细小病毒自然感染病例进行了临床观察、病理剖检及病理组织学观察,结果显示2病例均以犬细小病毒肠炎综合征为主要特征。表现为食欲废绝,排番茄酱样粪便,肠道黏膜坏死,覆以红黄色黏糊状物;镜检肠绒毛缩短,肠黏膜上皮细胞坏死或脱落,肠腺萎缩,肠腺细胞核内可见包涵体,胞浆呈玻璃样变;心肌纤维萎缩,粗细不均,肌纤维间较松散,有少量出血,炎症变化不明显。     

水貂细小病毒的分离鉴定

用F65细胞从疑似传统性肠炎的病死貂肠内容物中分离出一株病毒。经免疫电镜观察、细胞培养物核内包涵体检查以及血凝抑制试验证实为水貂细小病毒。     

水貂细小病毒的分离鉴定

用F_(6s)细胞从疑似传染性肠炎的病死貂肠内容物中分离出一株病毒。经免疫电镜观察、细胞培养物核内包涵体检查以及血凝抑制试验证实为水貂细小病毒。     

犬细小病毒病的病理学观察

文章对一例吉娃娃幼犬细小病毒病肠炎综合征病例进行了病理学诊断和检查,发现肠道广泛坏死,有充血出血现象,心脏心肌柔软,凝血不良,心房扩张,且伴有慢性出血性肺炎.光镜下见肠绒毛上皮细胞广泛变性、坏死、脱落,肠腔中有大量脱落的绒毛上皮细胞和炎性渗出物,固有层有多少不等的炎性细胞浸润,肠腺和肠绒毛上皮均可见特征性的核内包涵体;心肌纤维也有程度不等的变性、坏死,炎症细胞浸润.     

禽腺病毒人工感染产蛋鸡生殖道器官的病理学观察

用禽腺病毒 EDS_(76)H_(91-1)和 EDS_((?)6)Y_(81)G_4人工感染8只SPF 产蛋鸡和32只伊莎蛋鸡,5天后出现 HI 抗体,第4天后蛋壳颜色变浅,并出现软壳蛋、薄壳蛋、畸形蛋等.在感染后第3～20天内不同时期分别扑杀,取输卵管和卵巢经普通光镜、扫描电镜、透射电镜病理组织学观察,可见卵巢的生殖上皮细胞变性、坏死、核异常,间质有炎性细胞浸润:输卵管粘膜上皮的纤毛变性、坏死,固有层水肿,有较多瘤性细胞浸润;峡部粘膜上皮细胞出现核内包涵体;子宫部的固有层也有较多的炎性细胞,其蛋壳腺有萎缩现象,其结果证实了病毒主要集中在生殖道,输卵管和卵巢是该病毒侵害的主要部位。     

藏獒和松狮犬犬瘟热的病理学观察

对藏獒和松狮犬的犬瘟热自然感染病例进行了临床观察、尸体剖检以及病理组织学检查.结果显示,病毒主要侵害犬的呼吸、消化、神经、心血管和免疫系统.肺脏呈严重的间质性肺炎和支气管肺炎的变化,肺泡壁结构消失,肺泡腔内有大量巨噬细胞;胃、肠黏膜充血、水肿,上皮细胞坏死、脱落;脑膜和实质充血、水肿,可见微血栓形成;心脏明显扩张,右心肥大,心室腔内有鸡脂样凝血块;免疫器官受损严重,脾脏和淋巴结均呈明显退行性病变.在胃腺上皮细胞、肝细胞、肺泡上皮细胞和细支气管上皮细胞内发现嗜酸性的核内或胞浆包涵体.     

腺病毒引起放牧育成牛出血性肠炎

1990年10月在新泻县南部某牧场的45头放牧牛中有1头10月龄的黑白花母牛出现出血性下痢和脱水症状,随后死亡。剖检可见回肠及结肠内有鲜红色水样—粥状粪便贮留,肠粘膜充(出)血、浆膜和肠系膜水肿,系膜淋巴结明显肿大。组织学检查:肠道呈出血性肠炎,粘膜下层及粘膜下组织的血管内皮细胞有两性染色的核内包涵体,核内包涵体也在肠系膜淋巴结、肾及脾脏的血管内皮中出现。对包涵体用酶标抗体法试验,可知对牛腺病毒1、3及7型家兔免疫血清呈阳性反应。可是,没有见到血清间稀释倍数有差距,用酶标抗体法鉴别其血清型是困难的。用透射型电子显微镜检查,可见到在肠粘膜下层的血管内皮细胞的核内有呈结晶状排列的病毒粒子。     

小猪腺病毒性肠炎

用6618腺病毒株,对剖腹产取出的未吮初乳的小猪进行实验感染。经过3—4天潜伏期后,被感染的小猪全部出现腹泻。病理组织学检查,在空肠的后部和回肠里的短绒毛上,存在着许多核内包涵体。用电镜检查,可见包涵体含有多个腺病毒颗粒。肠内容物阴性染色、也发现了腺病毒颗粒。在空肠末端和回肠的短绒毛上,看到了免疫过氧化物酶阳性细胞。用上述技术,对一头小猪(自然发生感染)进行了腺病毒性肠炎研究,看到了与实验小猪相似的肠内损害。     

猪细胞巨化病毒的分离

1984年5月,北海道綱走支厅北见市内的一个养猪场,14窝135头6—25日龄仔猪发生了以打喷嚏为特征的疾病。病猪的鼻腔内充满粘稠鼻液。病理组织学检查,发现鼻腔内粘液腺上皮细胞肿大和核内包涵体形成。电子显微镜观察时发现病变部有疱疹病毒样粒子存在,故诊断为包涵体     

海狸鼠消化管显微及亚显微结构

应用光镜、电镜和组织化学技术,对 １０ 只成年海狸鼠消化管的食管、胃底、小肠和大肠壁的显微和亚显微结构进行了研究。结果显示,在 Ｈ Ｅ 染色,海狸鼠食管粘膜上皮细胞角化程度较高,胃底腺壁细胞的数量几乎与主细胞的相等或稍多,小肠肠腺底部含有大量潘氏细胞; Ｓｃｈｉｆｆ 氏染色,胃粘膜的上皮细胞、胃底腺的颈粘液细胞、十二指肠腺的粘液细胞、肠腺的潘氏细胞和杯状细胞均为阳性; Ｍ ａｓｓｏｎｆｏｎｔａｎａ 氨银法染色,在胃底腺和肠腺内均见有银亲合细胞。扫描电镜下,胃粘膜表面见有较多胃小凹,小肠上皮细胞的微绒毛形成许多指状突起。透射电镜观察,胃底部壁细胞中线粒体、滑面内质网、细胞内小管发达,小肠上皮细胞的微绒毛密集排列,细胞间见有连接复合体结构,胃底腺和肠腺内见有散在分布的内分泌细胞。     

Immunohistological diagnosis of rabbit haemorrhagic disease in experimentally infected rabbits in Spain.

The immunoreactivity of routinely processed liver and lung tissue samples obtained from rabbits inoculated with tissue explants from naturally infected animals when antisera directed against parvovirus from different species (canine, feline and porcine) as well as a RHD virus antiserum were employed has been tested by different immunoperoxidase methods. Cross-reactivity between RHD-virus antigens and parvovirus antigens was present. Best results were obtained with RHD and canine parvovirus antisera with the ABC method. The immunoreactivity in the liver was found in hepatocytes, Kupffer and bile duct cells. In the lung, it was exclusively observed in intravascular macrophages.     

Comparisons of feline panleukopenia virus, canine parvovirus, raccoon parvovirus, and mink enteritis virus and their pathogenicity for mink and ferrets

Parvoviruses from mink (mink enteritis virus [MEV]), cats (feline panleukopenia virus [FPV]), raccoons (raccoon parvovirus [RPV]), and dogs (canine parvovirus [CPV]) were compared. Restriction enzyme analysis of the viral replicative-form DNA revealed no consistent differences between FPV and RPV isolates, but CPV and MEV isolates could be distinguished readily from other virus types. Feline panleukopenia virus, RPV, and MEV, but not CPV, replicated to high titers in mink. However, on the first passage, disease and microscopic lesions were observed only in mink inoculated with MEV. Feline panleukopenia virus and RPV isolates replicated in ferrets, but disease or microscopic lesions were not observed. Feline panleukopenia virus and RPV isolates could be passaged repeatedly in mink and ferrets. Virulence of FPV and RPV isolates was low compared with that of MEV, and only a single mink inoculated with FPV or with RPV developed clinical disease on the sixth passage of virus.     

Experimental parvovirus infection in dogs.

Five eight week old dogs were inoculated orally and intranasally with cell culture origin canine parvovirus. Three dogs became depressed and anorectic and developed a mild (one dog) to severe diarrhea five days postinfection. The remaining dogs had subclinical infections but developed a lymphopenia followed by a transient lymphocytosis. The ill dogs developed mild (one dog) to severe neutropenia and a moderate lymphopenia. One died nine days postinfection. Recovery was associated with cessation of viral excretion and with lymphocytosis and antibody production. Two of three dogs challenged intragastrically developed mild clinical signs and a moderate panleukopenia four to eight days postinfection. The pathological changes of the experimental disease were very similar to that of spontaneous disease. Bone marrow changes included a severe granulocytic and mild erythroid depletion. The pathogenesis of canine parvovirus infection is discussed.     

Canine parvovirus enteritis 3: Scanning electron microscopical features of experimental infection

A group of 10-week-old puppies was orally inoculated with canine parvovirus of faecal origin. Scanning electron microscopy was used to study and compare the surface topography in both control and inoculated animals. In control dogs the villi were tall and finger-like in shape and numerous irregular transverse circumferential grooves were present on the surface. At higher magnification, the outlines of individual epithelial cells and depressions, interpreted as goblet cells, could be discerned. In the inoculated dogs, scanning electron microscopy changes were first seen at six days after inoculation. The small intestinal mucosa was covered by a thick layer of mucus. The underlying villi were stunted and had lost their surface features. In some instances there was loss of the luminal epithelium, exposing the lamina propria. In addition, there was dilation of the circumvillar basins and the crypt mouths. There appeared to be regenerative changes by day 7 after inoculation. The surface of the small intestinal mucosa was still covered by a thick layer of mucus. Where villi could be discerned, they were short and pointed and transverse grooves could be seen on their surface. There was some hypertrophy of the intervillus ridges. The changes in the surface topography of the small intestinal mucosa following canine parvovirus infection are compared to those seen in enteric infections in other species and the similarity of the lesion to that seen following sublethal irradiation is discussed.     

Clinical, virologic, and histopathologic observations of induced porcine parvovirus infection in boars

Twelve 8- to 12-month-old crossbred boars were inoculated with a virulent strain (NADL-8) of porcine parvovirus (PPV). Hemicastrations were performed on 6 boars 3, 7, 10, 14, 21, and 28 days after an IM injection of 10(8) median cell culture infectious dose (CCID50) of PPV (n = 3) or injection of 10(7.4) CCID50 given intratesticularly (IT, n = 3). Noninfected cell culture medium (0.25 ml) was injected into each testicle of a 7th boar (IT inoculated control). Virus or viral antigen was detected in testicular and epididymal tissues up to 14 days after inoculation. Direct immunofluorescence indicated that viral antigen was mainly associated with the vasculature of the interstitium. Microscopic lesions were not evident in the testicles and epididymides of IM inoculated boars. Acute-to-chronic testicular degeneration was evident in the IT inoculated boars, as well as in the IT inoculated control boar. Six boars were inoculated IM or orally/nasally with 10(7.9) CCID50 of PPV. Semen was collected twice weekly for 8 weeks after inoculation. Virus was not detected in any ejaculates. Semen also was collected from 4 boars for 5 weeks before inoculation, and preinoculation and post-inoculation semen quality was compared. Pronounced changes in sperm output, ejaculate volume, motility, or morphologic defects were not observed. The reproductive consequences of experimental PPV infection in boars were minimal because reproductive function was unaffected and venereal transmission of PPV was not detected.     

犬细小病毒病原分离及分型研究

为查明4份疑为患细小病毒病军犬的病原及其特性,为进一步的免疫研究奠定基础,本试验将4份送检的犬肠道内容物过滤后分别接种猫肾细胞(F81),培养5 d后,未出现细胞病变的带毒盲传。同时提取病料的总DNA,用犬细小病毒的VP2特异性引物进行PCR扩增,PCR阳性产物克隆至pMD18-T载体测序,并与已知参考毒株序列进行比对及系统发育分析。测序结果表明,用F81细胞分离到4株细小病毒;经VP2基因比对分型结果表明,4株细小病毒毒株均属CPV-2a,分别命名为CPV-JQ、CPV-CM、CPV-M和CPV-KM。     

A sequential study of experimental infection of pigs with porcine circovirus and porcine parvovirus: immunostaining of cryostat sections and virus isolation

The sequential tissue distribution of virus was investigated using virus isolation and immunofluorescence tests in 1-day-old piglets inoculated with porcine circovirus 2 (PCV2) and/or porcine parvovirus (PPV). Enlarged mesenteric lymph nodes were seen in the pig inoculated with PCV2 alone and killed at 26 days post-inoculation (PI). One of the pigs inoculated with PCV2 and PPV and killed at 21 days PI had an enlarged liver. The pig killed at 26 days PI in this group had enlarged liver, kidneys and heart. Histopathological changes were seen in lymphoid tissues of the pigs inoculated with PCV2 alone and killed at 14 and 26 days PI. Similar, but more severe, lesions were observed in the pigs infected with PCV2 and PPV and killed from 10 days PI onwards. Histological lesions of nephritis, pneumonia and hepatitis were also apparent in these animals. Mild nephritis was also seen in the pigs infected with PPV alone and killed at 14 and 26 days PI. Moderate amounts of PPV antigen were detected in tissues from the pigs inoculated with PPV alone and killed at 14 days PI. Low levels of PCV antigen were detected, mainly in lymphoid tissues, in the pigs inoculated with PCV alone and killed at 14 days PI. Low to moderate amounts of PCV antigen were detected in a wider range of tissues in the pig in this group killed at 26 days PI. In the pigs inoculated with both viruses, PPV antigen was detected in tissues of pigs killed from 3 to 26 days PI with maximal amounts detected between 6 and 14 days PI. PCV2 antigen was detected in low to moderate amounts in the tissues of pigs killed at 14 days PI. Large amounts of PCV2 antigen were detected in most of the tissues from pigs in this group killed between 17 and 26 days PI. Virus isolation results for PCV2 generally correlated well with the results for immunofluorescent staining. PPV was isolated from almost all tissues from pigs inoculated with PCV2 and PPV, a much higher incidence of positive tissues than observed for immunofluorescent staining.     

水貂肠炎细小病毒灭活疫苗抗体消长规律的研究

应用血凝抑制试验对水貂肠炎细小病毒灭活疫苗免疫水貂进行抗体水平动态监测,结果表明,疫苗接种14 d抗体达到保护,21~30 d抗体水平达到高峰;免疫180 d抗体仍在保护值以上。攻毒试验证实,免疫180 d后90%免疫水貂获得保护,确定水貂细小病毒性肠炎灭活疫苗免疫保护期可持续6个月。     

Response of mink, skunk, red fox and raccoon to inoculation with mink virus enteritis, feline panleukopenia and canine parvovirus and prevalence of antibody to parvovirus in wild carnivores in Ontario.

Mink virus enteritis, feline panleukopenia and canine parvovirus-2 were inoculated separately into groups of raccoon, mink, red fox and striped skunk. Raccoons were highly susceptible to mink virus enteritis and feline panleukopenia, with animals developing clinical illness, and several dying within six to ten days of inoculation with lesions typical of parvovirus infection. Both viruses were shed in high titre in the feces of infected raccoons, and high antibody titres were stimulated. Raccoons inoculated with canine parvovirus-2 showed no signs; shedding of virus was sporadic though moderate titres of antibody developed. Mink inoculated with mink virus enteritis and feline panleukopenia developed signs and lesions of early parvovirus infection. No signs or significant lesions followed canine parvovirus-2 inoculation. Shedding of virus was heavy (mink virus enteritis) or sporadic (feline panleukopenia and canine parvovirus-2), though good serological responses were elicited to all three viruses. Red fox showed no signs of infection, shed all three viruses only sporadically, and the serological response was strong only to feline panleukopenia. Skunks developed low antibody titres, but no signs, and did not shed virus. Antibody to parvovirus was found in 79.2% of 144 wild red foxes; 22.3% of 112 wild raccoons; 1.3% of 157 wild skunks and 6/7 coyotes in southern Ontario. The likely significance of these viruses to wild and captive individuals and populations of these carnivores is discussed.     

犬细小病毒HZ0761株的分离与鉴定

采集疑似细小病毒(CPV)感染犬的粪便,采用同步培养法接种胎猫肾细胞(F81)进行病毒分离鉴定。通过PCR检测、HA试验、IFA鉴定、电镜观察和空斑纯化,获得1株犬细小病毒,并命名为HZ0761。感染的F81细胞48h后出现明显的细胞病变;在病料和感染的F81细胞中均扩增出CPV VP2基因的特异性片段(221 bp);病毒液可凝集猪红细胞,血凝价为1∶28,其血凝性能被特异性抗体抑制;IFA可见特异性亮绿色荧光;电镜观察感染的F81细胞核内可见20 nm左右的病毒颗粒;病毒液的TCID50为10-4.8/mL,VP2基因序列分析显示该毒株为CPV-2 a型。