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PubMed1985

Epizootics of respiratory tract disease in swine in Belgium due to H3N2 influenza virus and experimental reproduction of disease.

In Belgium, influenza virus was isolated from swine in 22 epizootics of respiratory tract disease in swine during 1984. In 8 of the epizootics, H3N2 influenza virus, related to the A/Port Chalmers/1/73 strain, was isolated. Intratracheal inoculation of the isolates induced clinical signs. It was concluded that the A/Port Chalmers/1/73 strain was established in the Belgian swine population and was responsible for the epizootics of respiratory tract disease in swine.

Animals↗
PubMed2000

Singleton reactors in the diagnosis of swine vesicular disease: the role of coxsackievirus B5.

Swine vesicular disease virus (SVDV) and Coxsackie B5 virus (CVB5) are closely related viruses that can infect swine and man and give rise to cross-reacting serum antibodies. It is, therefore, possible that SVD antibodies found in serologic screenings of pigs are induced by CVB5. Single positive animals found in screening programmes are generally referred to as singleton reactors (SR). To determine whether SR in SVDV screenings are induced by CVB5 infection, virus neutralisation tests (VNTs) and radioimmunoprecipitation assays (RIPA) were carried out on sera of SR, sera of pigs experimentally infected with SVDV, and sera from pigs vaccinated with CVB5 isolates. The SR sera reacted repeatedly positive in the SVDV UKG/27/72 VNT, but reacted differently in three other VNTs (SVDV NET/1/92, CVB5A, and CVB5B). The VNT titres obtained with the SR sera revealed a correlation between both SVDV strains, and also between both CVB5 stains, but no correlation was found between SVD and CVB5 VNT titres. Sera of experimentally infected (SVDV) or vaccinated (CVB5) pigs showed titres in all four neutralisation tests. In the RIPA, the reaction patterns of the SR sera varied considerably with all four antigens used, in contrast to sera from pigs experimentally infected with SVDV that reacted with all antigens used, and sera from pigs vaccinated with CVB5 that reacted only with CVB5 antigens. The results presented in this paper show that neither CVB5 nor SVDV infections are the only cause of the SR phenomenon. Testing for CVB5 specific antibodies can reduce the number of SR sera in the serodiagnosis of SVDV.

Animals↗
PubMed1975

Brain and spinal cord lesions in pigs inoculated with swine vesicular disease (UKG strain) virus and coxsackievirus B5.

Pigs inoculated intravenously with swine vesicular disease virus (UKG strain), those inoculated with coxsackievirus B5, and other pigs exposed by pen contact to the same viruses developed diffuse encephalomyelitis. Perivascular cuffing, with lymphocytes and formation of neuroglia cell foci, were most prominent in telencephalon, diencephalon, and mesencephalon. Encephalitis was of mild to severe intensity. Severity of lesions was more extensive and severe in the pigs exposed to swine vesicular disease virus. Pen contact exposure to either of the 2 viruses caused a more severe central nervous system reaction than did intravenous inoculation. The type and the distribution of lesions produced by the 2 viruses indicate that they may be related.

Animals↗
PubMed2000

Swine vesicular disease virus. Pathology of the disease and molecular characteristics of the virion.

Swine vesicular disease is a highly contagious disease of pigs that is caused by an enterovirus of the family Picornaviridae. The virus is a relatively recent derivative of the human coxsackievirus B5, with which it has high molecular and antigenic homology. The disease is not severe, and affected animals usually show moderate general weakening and slight weight loss that is recovered in few days, as well as vesicular lesions in the mucosa of the mouth and nose and in the interdigital spaces of the feet. However, the similarity of these lesions to those caused by foot-and-mouth disease virus has led to the inclusion of this virus in list A of the Office International des Epizooties. The disease has been eradicated in the European Union except in Italy, where it is considered endemic in the south. Nevertheless, as occasional outbreaks still appear and must be eliminated rapidly, European countries are on the alert and farms are monitored routinely for the presence of the virus. This circumstance has led to a considerable effort to study the pathology of the disease and the molecular biology and antigenicity of the virus, andto the development of optimized methods for the diagnosis of the infection.

Animals↗
PubMed1990

The complete nucleotide sequence of a pathogenic swine vesicular disease virus.

The nucleotide sequence of a swine vesicular disease virus (SVDV) strain that is pathogenic for pigs has been determined and compared with that of a non-pathogenic strain of SVDV, as well as a number of other enteroviruses. It shows only 98 base changes in comparison with a non-pathogenic strain of SVDV (Inoue et al., 1989, J. Gen. Virol. 70, 919-934). Fourteen of these nucleotide differences between the pathogenic and the non-pathogenic SVDV strains occur in the 5' non-coding region which, by analogy with the other picornaviruses, has been implicated in the efficiency with which the RNA is employed as mRNA. Additional differences found throughout the coding regions are largely conservative in nature. A number of residues are discussed as candidates for determinants of pathogenicity. This sequence has been submitted to the PIR database and has accession number A30061.

Amino Acid Sequence↗
PubMed2003

Crystal structure of Swine vesicular disease virus and implications for host adaptation.

Swine vesicular disease virus (SVDV) is an Enterovirus of the family Picornaviridae that causes symptoms indistinguishable from those of foot-and-mouth disease virus. Phylogenetic studies suggest that it is a recently evolved genetic sublineage of the important human pathogen coxsackievirus B5 (CBV5), and in agreement with this, it has been shown to utilize the coxsackie and adenovirus receptor (CAR) for cell entry. The 3.0-A crystal structure of strain UK/27/72 SVDV (highly virulent) reveals the expected similarity in core structure to those of other picornaviruses, showing most similarity to the closest available structure to CBV5, that of coxsackievirus B3 (CBV3). Features that help to cement together and rigidify the protein subunits are extended in this virus, perhaps explaining its extreme tolerance of environmental factors. Using the large number of capsid sequences available for both SVDV and CBV5, we have mapped the amino acid substitutions that may have occurred during the supposed adaptation of SVDV to a new host onto the structure of SVDV and a model of the SVDV/CAR complex generated by reference to the cryo-electron microscopy-visualized complex of CBV3 and CAR. The changes fall into three clusters as follows: one lines the fivefold pore, a second maps to the CAR-binding site and partially overlaps the site for decay accelerating factor (DAF) to bind to echovirus 7 (ECHO7), and the third lies close to the fivefold axis, where the low-density lipoprotein receptor binds to the minor group of rhinoviruses. Later changes in SVDV (post-1971) map to the first two clusters and may, by optimizing recognition of a pig CAR and/or DAF homologue, have improved the adaptation of the virus to pigs.

Adaptation, Physiological↗
PubMed1983

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.

Animals↗
PubMed1974

Experimental edema disease of swine (E. coli enterotoxemia). II. The development of hypertension after the intravenous administration of edema disease principle.

The intravenous inoculation of edema disease principle induced profound hypertension in pigs. The increase in blood pressure occurred approximately 40 hours after inoculation and coincided with the development of the characteristic neurological disturbance of edema disease. Therefore hypertension may play a pathogenetic role in the neuropathy of experimental edema disease.

Animals↗
PubMed1974

The airborne excretion by pigs of swine vesicular disease virus.

The air of loose-boxes holding pigs affected with swine vesicular disease was sampled for virus. In the multistage impinger virus to a titre of 10(2.6) TCID 50 was associated with particles greater than 6 mum., 10(1.6) with particles 3-6 mum. and 10(1.4) or less with particles less than 3 mum. In the noses of workers in contact with the pigs for periods not less than 5 min., virus to a titre of 10(2.4) TCID 50 was found. Virus was recovered from the air for 2-3 days during the disease and maximum titre in pigs infected by injection or by contact occurred on the second to third day after generalization of the lesions. The amounts of virus were about 160-fold less than those recovered from pigs affected with foot-and-mouth disease, and the quantity and time of excretion suggest that the source of swine vesicular disease virus in the aerosol may be from the lesions and skin rather than from the respiratory tract.

Air Microbiology↗
PubMed1998

A RT-PCR assay for the differential diagnosis of vesicular viral diseases of swine.

A RT-PCR assay based on specific amplification of RNA sequences from each of the etiological agents of three important vesicular diseases that affect swine, foot-and-mouth disease virus (FMDV), swine vesicular disease virus (SVDV), and vesicular stomatitis virus (VSV), was developed. Genotype-specific primers that amplified DNA fragments of differential size from SVDV 3D gene or VSV L gene were selected with the aid of a computer program. Experimental testing of the primers predicted as SVDV-specific identified a primer pair, SA2/SS4, that rendered a specific product from SVDV RNAs, but did not amplify RNA from either FMDV or coxsackie B5 virus (CV-B5), a highly related picornavirus. Primers SA2/SS4 were used in combination with primers 3D2/3D1, which amplify a product of different size on FMDV 3D gene (Rodriguez et al., 1992). This combined RT-PCR reaction allowed a sensitive and specific differential detection of FMDV and SVDV RNAs in a single tube, by means of the analysis of the amplified products in agarose gels. The results obtained were similar when RNA extracted from viral stocks or plastic wells coated with either viral supernatants or extracts from lesions of infected animals, were used as starting material in the reactions. Using a similar approach, VSV serotype-specific primers IA/IS and NA/NS were selected for the specific amplification of VSV-Indiana and VSV-New Jersey RNAs, respectively. The combined use of SVDV, FMDV and VSV specific primers in a single reaction resulted in a genotype-specific amplification of each of the viral RNAs. Thus, differential diagnosis of FMDV from SVDV and/or VSV can be carried out in a single RT-PCR reaction, using a rapid and simplified methodology.

Animals↗
PubMed1982

Counter immunoelectrophoresis in the diagnosis and serological surveillance of swine vesicular disease.

A comparison of the counter immunoelectrophoresis (CIEP) test for swine vesicular disease with serum neutralisation and double immunodiffusion is reported here. Two groups of sera were used in the comparison: one group (908 sera) was tested blind by CIEP and the other group (778 sera) comprised field samples from infected and suspect premises submitted routinely for swine vesicular disease confirmation. The CIEP test proved simple to perform and gave results within two hours. It was very economic in the use of reagents and its sensitivity, though less than that of the serum neutralisation test, compared favourably with the sensitivity of the double immunodiffusion test. No false positive results were detected out of the 1686 sera tested.

Animals↗
PubMed1979

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.

Animals↗
PubMed1976

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.

Animals↗
PubMed2004

Use of automated real-time reverse transcription-polymerase chain reaction (RT-PCR) to monitor experimental swine vesicular disease virus infection in pigs.

Automated real-time RT-PCR was evaluated as a diagnostic tool for swine vesicular disease virus (SVDV) infection on a range of samples (vesicular epithelium, serum, nasal swabs, faeces) from four inoculated and three in-contact pigs over a period of 28 days. Traditional diagnostic procedures (virus isolation, and ELISAs for antigen and antibody) were used in parallel. Each inoculated pig developed a significant viraemia and clinical disease, and excreted virus, which was transmitted to the in-contact animals. The latter, however, developed only a short-lived, low-level viraemia and no clinical disease. The RT-PCR and virus isolation were generally comparable in detecting SVDV in the serum and nasal swabs from inoculated and in-contact pigs up to day 6 after infection; it was possible, however, to isolate virus for a longer period from the faeces of a few pigs. This suggested that further optimization of the template extraction method was required to counteract the effects of RT-PCR inhibitors in faeces. It was concluded that the automated real-time RT-PCR is a useful diagnostic method for SVD in clinically or subclinically affected pigs and contributed to the study of the pathogenesis of SVD in the pigs.

Animals↗