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.     

Comparative studies of United Kingdom isolates of swine vesicular disease virus

The characteristics of four United Kingdom isolates of swine vesicular disease (SVD) virus from 1981 to 1982 have been compared with those of an isolate obtained from the first outbreak of swine vesicular disease diagnosed in the United Kingdom in 1972. When the virus structural proteins were examined by polyacrylamide gel electrophoresis the four isolates from 1981-82 all had the same polypeptide pattern, which was different from that of the 1972 isolate. Immunodiffusion tests with the 1972 isolate and one 1982 isolate did not reveal any antigenic difference between the viruses but minor antigenic differences were shown by cross-neutralisation tests between the 1972 isolate and the four isolates from 1981-82. In experimentally infected pigs the 1972 isolate produced typical SVD lesions whereas the four more recent SVD viruses produced only very mild clinical disease. Clinical lesions scored numerically were four- to 10- and five- to 11-fold higher at seven and 14 days after infection for pigs infected with the 1972 isolate than with the four isolates from 1981-82. The serum of pigs infected with the 1972 isolate contained significantly higher levels of neutralising antibody than those of pigs infected with more recent isolates. The antibody titres of pigs with only primary lesions ranged from log10 1.9 to 2.8 and one clinically normal pig had a titre of log10 2.4 at 14 days after infection. Attention is drawn to the implication of these findings for SVD control policies based only on the recognition and reporting of clinical disease.     

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.     

猪水泡病病毒的分子生物学研究进展

猪水泡病(Swine vesicular d isease,SVD)是猪的一种高度接触性传染病,其临床表现以口鼻腔粘膜、蹄部等出现水泡或溃烂为特征,与猪口蹄疫极其相似,常以流行形式发病,对养猪业的危害较大,因而其防治问题极受重视,世界动物卫生组织(OIE)将其列为动物A类传染病。猪水泡病病毒(Swin     

Radial immuno-diffusion and serum-neutralisation techniques for the assay of antibodies to swine vesicular disease.

Pig sera were assayed for antibodies to swine vesicular disease virus by (a) the radial immuno-diffusion technique combined with autoradiography and (by serum neutralisation tests. The former was more sensitive and was used for initial screening of sera while the latter was used to obtain estimates of titres of positive sera. In a survey of 1759 sera collected at slaughterhouses there were 14 significant titres from a total of seven premises situated in localities where the disease had been known to occur, and it was concluded that this did not indicate wither widespread undetected disease or the occurence of inapparent infection in the pig population.     

Detection of swine caliciviruses by indirect immunofluorescence.

The indirect immunofluorescence test is a rapid method for detecting the presence of vesicular exanthema of swine virus or San Miguel sea lion virus in cell culture. A serological relationship exists between vesicular exanthema of swine virus and San Miguel sea lion virus, as shown by the fluorescence-positive reactions between swine antisera to vesicular exanthema of swine virus A48 and San Miguel sea lion virus type 5 and cell cultures infected with San Miguel sea lion virus types 1, 2, 3, 4 and 5 as well as vesicular exanthema of swine virus B51, C52, D53, E54, F55, G55, H55, I55, J56 and K55. The indirect immunofluorescence test detects group-specific antibody to caliciviruses in swine sera.     

A study of swine dysentery by immunofluorescence and histology.

Twenty-six specific-pathogen-free pigs were fed pure cultures of Treponema hyodysenteriae. Five untreated pigs were controls. Distribution of this large spirochete in pigs with swine dysentery was shown by the indirect fluorescent antibody technique. Findings by this method were compared with those from dark-field examination of colonic mucosal scrapings and from tissue sections. The cultures caused mucohemorrhagic colitis which by 10 days after inoculation was indistinguishable from the colitis of swine dysentery. Control pigs remained normal. Pigs killed when spirochetes were first seen in the feces had normal colonic mucosa with only a few spirochetes. At the first sign of diarrhea, however, the colonic mucosa was thicker than normal and had many spirochetes. T. hyodysenteriae was confined to regions of hypertrophy and exudation of the large intestine mucosa throughout the course of disease.     

Experiments on the preparations and testing of associated vaccine against foot and mouth disease and vesicular disease in swine.

Tests for associated immunization of swine against Foot and Mouth Disease (FMD) and Vesicular Disease (SVD) of swine were carried out. As a result of this investigation, it was established that the prepared and tested inactivated oil vaccine is harmless and immunogenic in sensitive animals. In investigating the course of immunity, the presence of antibody against both antigens was demonstrated in vaccinated animals. All once-vaccinated animals were defended against the virus of SVD during challenge, and 75% of them were defended against FMD. After revaccination, all immunized swine were defended against infection with both viruses. The question of the quality of the associated vaccine and the possibilities of its massive use in industrial swine rearing was discussed.     

No serological evidence for the presence of swine vesicular disease virus in South Africa.

An indirect ELISA incorporating a protein A-peroxidase conjugate was developed for detecting antibodies to swine vesicular disease virus (SVDV) in pig sera. This test and a conventional virus neutralization test were found to be equally sensitive. A total of 2846 pig sera collected from various abattoirs in South Africa were tested using the indirect ELISA. No serological evidence of infection with SVDV in pigs in South Africa was found.     

Experimental vesicular stomatitis virus infection of swine: Extent of infection and immunological response

Swine, a natural host species for infection by vesicular stomatitis virus (VSV), were infected with VSV-New Jersey (VSV-NJ) serotype virus obtained from a recent field isolate. Tissues collected from the infected pigs were examined for the presence of infective virus, for viral antigens, and/or for viral nucleic acid. Infective virus could be recovered from tissues near the site of infection for as long as 6 days after the primary infection with VSV. However, no infective virus was recovered following hypothermia induced 11 weeks after infection, or following a secondary challenge with virus 22 weeks after initial infection. Immunofluorescence tests for viral antigens and nucleic acid hybridization assays failed to detect viral antigens or nucleic acids in tissues from which no infective virus could be recovered. Titers of serum-neutralizing antibody peaked 3–5 weeks after infection and then fell slightly until the secondary infection which caused a rapid anamnestic response. Peripheral blood mononuclear cells (PBM) tested 3, 5, 8 or 18 weeks after primary infection all produced readily detectable antigen-specific proliferative responses when cultured with VSV. Thus, although direct tests failed to demonstrate persistence of virus after infection, the humoral and cellular immune response remained elevated for months. Infective VSV was not required to stimulate the proliferative response since UV-inactivated VSV was immunogenic in these in vitro tests. Following primary infection, antigen-specific proliferative responses could be stimulated by several strains of VSV-NJ, but not by VSV-Indiana (VSV-Ind) serotype virus. Secondary infection had relatively little effect on the proliferative response to VSV-NJ strains, but it did cause the PBM to gain responsiveness to VSV-Ind.     

Swine vesicular disease, studies on pathogenesis, diagnosis, and epizootiology: a review

Swine vesicular disease (SVD) is a contagious viral disease of swine. It causes vesicular lesions indistinguishable from those observed of foot-and-mouth disease. Infection with SVD virus (SVDV) can lead to viraemia within 1 day and can produce clinical signs 2 days after a pig has come into contact with infected pigs or a virus-contaminated environment. Virus can be detected 3.5 hours after infection using immunohistochemistry. In these in vitro studies, this technique was superior to in-situ hybridization. In SVDV-infected tissues, however, more infected cells were positive using in-situ hybridization, and these were already seen 4.5 hours after infection. For serological diagnosis of SVD several new enzyme-linked immunosorbent assays (ELISA's) have been developed. The newest ELISAs, based on monoclonal antibodies, are superior to the previous tests. The new tests produce fewer less false-negative results and enable large-scale serological screening. In screening programmes a small percentage of false positive reactors have been detected. The cause of these false-positive reactions has not been identified, though infections with human Coxsackie B5 virus can be excluded.