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PubMed1990

Production of infectious swine vesicular disease virus from cloned cDNA in mammalian cells.

Full-length cDNA clones of the swine vesicular disease virus (SVDV) were constructed from subgenomic cDNA clones in the expression vector pSVL (pSVLS00). The direct transfection of mammalian cells with plasmid pSVLS00 results in the production of infectious virus. The recovered virus was neutralized completely by anti-SVDV guinea-pig serum, but did show a difference in plaque morphology from the parental virus.

Animals↗
PubMed1997

Intramural coronary artery disease in swine with naturally occurring hypertrophic cardiomyopathy.

Intramural coronary artery disease (ICAD) has been reported in myocardium affected with hypertrophic cardiomyopathy (HCM), but has never been studied in detail with respect to the cell type or lipid infiltration involved in the wall-thickening. The lack of heart samples may be one of the rationales to hamper the progress in investigating this disease. Recently, the discovery of naturally occurring HCM in swine has provided an excellent opportunity for the study of ICAD because of the high prevalence of ICAD in this animal. The present study provides a detailed structure feature in the thickened arterial wall of ICAD by both histologic and electron microscopic means. Morphologically, the feature of ICAD is due primarily to the neointimal thickening. Smooth muscle cells (SMC) and extracellular matrix (collagen and elastic fibers) are the major components responsible for the thickened neointima. Fragmentation of the internal elastic membrane is associated with the migration and proliferation of SMC from the media to the intima. Therefore, pigs with HCM may be a potential animal model not only for the study of the mechanism by which SMC migrate and proliferate into intima, but also for the future investigation of interventions in coronary artery occlusion.

Animals↗
PubMed1996

Fine surface structure of enterotoxemic Escherichia coli O139:K12 strains associated with swine edema disease.

The fine structure of the cell surface of seven enterotoxemic Escherichia coli (ETEEC) O139:K12 strains isolated from piglets with edema disease were examined electron microscopically using both the negative-staining method and the freeze-substitution fixation method. Densely packed, fine fibers were observed; they consisted of a capsule layer approximately 25 nm thick around the cell surfaces of strains 107/86, IW-2, ED-3, ED-43, and ED-61, all of which have a capacity to adhere strongly to HEp-2 cells. In contrast, no such structure was observed on the surface of strains RK-O139 or ED-1, both of which adhere only weakly to HEp-2 cells. These results suggest that the capsule structure might be associated with the ability to adhere to HEp-2 cells and, as a result, also potentially play some role in ETEEC infection.

Animals↗
PubMed2005

Utility of recombinant integrin alpha v beta6 as a capture reagent in immunoassays for the diagnosis of foot-and-mouth disease.

Recombinant integrin alpha v beta6 was evaluated as a capture ligand in a sandwich ELISA for the detection and serotyping of foot-and-mouth disease (FMD) virus. Our routinely applied method employs seven serotype-specific rabbit polyclonal antibodies as capture ligands and seven serotype-specific guinea pig polyclonal antibodies as detecting reagents. The recombinant integrin bound FMD virus of all seven serotypes but not that of another vesicular disease, swine vesicular disease (SVD). Considerable heterotypic cross-reactions were evident when using the integrin capture ligand in combination with guinea pig detecting antibodies but totally type-specific reactions resulted when serotype-specific monoclonal antibodies (mabs) were used instead of the guinea pig reagents. The specificity of reaction of the integrin capture/mab detector combination was superior to that of our routinely employed rabbit/guinea pig ELISA and offers an improvement for test interpretation. As a universal trapping reagent for all FMD virus serotypes the alpha v beta6 recombinant protein also has the potential for application in other test procedures for viral identification (e.g. pen-side chromatographic strip-tests, biosensors, immunocapture RT-PCR, antigenic characterization procedures and monoclonal antibody profiling of emerging field virus strains) and in antibody detection assays employed for the diagnosis of FMD.

Animals↗
PubMed2002

Characteristics of capsules in enterotoxemic Escherichia coli O139:K12 strains causing swine edema disease.

The characteristics of the capsule of the enterotoxemic Escherichia coli (ETEEC) O139:K12 strains that strongly adhere to Hep-2 cells were examined. Electron microscopic studies using the freeze-substitution technique revealed that ETEEC strains had a capsule of approximately 25 nm. These strains show hydrophobic surface properties and strong adherence to human polymorphonuclear leukocytes (PMNs). In contrast, ETEEC strains RK-O139 and ED-1 show weak adherence to HEp-2 cells and fail to express the capsule layer on the cell surface. These ETEEC strains possess hydrophilic surface properties and also adhere to PMNs. The lipopolysaccharide (LPS) analysis by means of sodium dodecyl sulfate polyacrylamide gel electrophoresis (SDS-PAGE) showed that ETEEC strains had the same LPS profile and long O-side chains of LPS. Furthermore, all strains were resistant to serum killing activity. These results suggest that the capsule of ETEEC strains does not contribute as an antiphagocytic factor, but as an adherence factor to host cells.

Animals↗
PubMed2001

Tetracycline resistance genes in isolates of Pasteurella multocida, Mannheimia haemolytica, Mannheimia glucosida and Mannheimia varigena from bovine and swine respiratory disease: intergeneric spread of the tet(H) plasmid pMHT1.

Tetracycline-resistant isolates of Pasteurella multocida and Mannheimia spp. from respiratory diseases in cattle and swine were investigated for the classes of tet gene and their chromosomal or plasmid location. The 34 isolates comprised eight P. multocida, 23 Mannheimia haemolytica, two Mannheimia varigena and a single Mannheimia glucosida isolate. Identification of the tet genes was achieved by PCR analysis and hybridization with specific probes. Transformation and hybridization experiments served to confirm the plasmid location of tet genes. Selected tet genes and their adjacent regions were sequenced. The tet genes tet(B), tet(G) and tet(H) were detected. The gene tet(H) was present in 26 isolates. The 4.4 kb tet(H)-carrying plasmid pMHT1 was detected in six isolates representing all four species. In the remaining 28 isolates, copies of tet(B), tet(G) and tet(H) were identified as chromosomal. No correlation between the tet gene type and the MIC of tetracycline, or between the number of tet gene copies and the MIC of tetracycline was observed. Tetracycline resistance in P. multocida and Mannheimia spp. is mediated by at least three different tet genes. A new type of tet(H)- carrying plasmid, pMHT1, was identified. The detection of pMHT1 in M. glucosida and M. varigena is the first report of resistance plasmids in isolates of these two species. For the first time, tet(G) genes were detected in members of the family Pasteurellaceae.

Animals↗
PubMed2003

Reduction of economic losses caused by mycoplasmal pneumonia of pigs by vaccination with Respisure and by Tiamutin treatment.

The possibilities and economic benefits of controlling mycoplasmal pneumonia of pigs caused by Mycoplasma hyopneumoniae by immunisation with Respisure and by Tiamutin treatment were studied. The experiment was carried out in a herd comprising 1000 sows which was free of PRRS, Aujeszky's disease, swine dysentery and leptospirosis, and the prevalence of mycoplasmal pneumonia was low because the farm had recently been restocked. Groups C1 and C2 served as untreated controls, while Groups R1 and R2 received a prestarter diet containing 100 ppm Tiamutin from the time of weaning. Piglets of Group R1 were vaccinated with Respisure vaccine once on day 69, while those of Group R2 twice, on days 65 and 80. Piglets of Groups ST1 and ST2 were fed 100 ppm Tiamutin in the diet for 7 days at the time of weaning and then at 4 months of age, while pigs of Group ST2 received such treatment also in the 6th month of life. The efficacy of treatment was analysed on the basis of the number of animals that died, were emergency slaughtered or were retarded in growth in the different groups, the body weight of animals at weaning, at 94 and 148 days of age and at the time of slaughter, their daily body weight gain, the lung lesions found in animals slaughtered from the different groups, the costs of medication and vaccination, and the cost-benefit calculations of the results. The mortality and emergency slaughter rate was 2.88% and 4.62% in Groups ST2 and ST1, respectively, 4.23% and 4.62% in Groups R2 and R1, respectively, and 8.39% and 9.44% in the control groups (C2 and C1, respectively). The rate of growth retardation was 0.48% and 2.12% in Groups R1 and R2, respectively, 1.59% and 3.46% in Groups ST1 and ST2, respectively, as compared to 8.03% and 6.55% in the control groups (C1 and C2, respectively). The severity score of lung lesions was 1.82 and 1.46 in Groups R1 and R2, 2.18 and 2.93 in Groups ST1 and ST2, and 3.83 and 4.02 in the control groups C1 and C2, respectively. The mean finishing weight of pigs was 102.4-107.8 kg and 95.2-106.6 kg in the treated groups and 94.5-98.6 kg in the control groups. The classification of pigs according to the EUROP categories showed a shift to the E and U categories in the treated groups. The average feed cost per one kg of liveweight was 77.89-82.64 Forints in the treated groups and 85.66 Forints in the control groups.

Animals↗
PubMed2006

Concurrent pathological and bacteriological findings in the urogenital organs and mammary glands of sows culled because of chronic vulvovaginal discharge and swine urogenital disease (SUGD): a case study.

The urogenital organs and mammary glands of sows, culled because of excessive vulval discharge, milking problems, and urogenital infections (swine urogenital disease, SUGD) in their history (n=1070 sows) were examined. The culled sows were assigned to three groups according to parity: parity 1 (n=356); 2-6 (n=354); and >6 (n=360). Necropsy findings associated with these groups were analysed separately. Bacteriological examination of vulval discharges was performed. Escherichia coli and a large number of Gram-positive and Gram-negative organisms were found in all samples of vulval discharge. Except ovarian degeneration and oedematous endometrium, older sows had more (P<0.05) pathological changes in the oviduct, ovaries, and uteri than younger (parity 1) sows. More (P<0.05) parity 1 sows had hyperaemic and congested vaginal walls and haemorrhages into the vaginal lumen than sows of higher parity, which suffered more (P<0.05) from accumulation of purulent material in the vaginal lumen, fibrinopurulent exudate adherent to the wall of the vagina, multifocal vaginal erosions and ulcerations, and purulent, mucopurulent or purulohaemorrhagic exudate in the vagina or on the cervix. Except acute pyelonephritis, mucosal hyperaemia, and congestion of the urinary bladder, more (P<0.05) sows of higher parity had pathological changes in their urinary organs. More (P<0.05) parity 1 sows had acute or chronic purulent exudative mastitis than sows of higher parity, which had more (P<0.05) mammary gland abscessation, mammary gland cysts, and fibrous mastitis. All parity 2-6 and >6 sows had mammary gland and bladder changes, parity >6 sows had changes in the kidney, and renal pelvis, and parity 1 sows had mammary gland changes. Most parity 1 sows had bladder, kidney, and renal pelvis alterations and most parity 2-6 animals had pathological kidney and renal pelvis changes.

Animals↗
PubMed1980

Swine vesicular disease viruses isolated from healthy pigs in non-epizootic period. II. Vesicular formation and virus multiplication in experimentally inoculated pigs.

An infection experiment was carried out on pigs with swine vesicular disease virus isolated from healthy pigs (SVDV-H). Inoculation was done by two routes, intradermal in the coronary band of the foot and oral. Observation was made on the formation of vesicles and their spread, the virus contents of serum, swab of the oral cavity, and feces, the vicissitude of neutralizing antibody titers, and the distribution of virus in the body. From its results the pathogenicity of virus was judged. In the pigs inoculated intradermally there was a difference in the extension of the area involved in vesicular formation between any two strains of virus. That is, vesicular formation was restricted to the site of inoculation, involved the site of inoculation and the sole of the hoof, or spread over the oral and nasal regions. In every pig, however, vesicles developed only for 2 approximately 5 days after inoculation. After that, repair progressed rapidly. Some strains caused viremia, which was mild. The virus was detected from the site of vesicular formation, but not from any organ. Neutralizing antibody began to be detected 3 days after inoculation. Its titer reached a plateau about 10 days later. In the pigs inoculated perorally, no vesicles were formed. The virus was only detected from the tonsils and the intestinal contents. These findings made it clear that SVDV-H was less pathogenic than swine vesicular disease virus isolated from diseased pigs.

Animals↗
PubMed2001

The N-terminal region of the VP1 protein of swine vesicular disease virus contains a neutralization site that arises upon cell attachment and is involved in viral entry.

The N-terminal region of VP1 of swine vesicular disease virus (SVDV) is highly antigenic in swine, despite its internal location in the capsid. Here we show that antibodies to this region can block infection and that allowing the virus to attach to cells increases this blockage significantly. The results indicate that upon binding to the cell, SVDV capsid undergoes a conformational change that is temperature independent and that exposes the N terminus of VP1. This process makes this region accessible to antibodies which block virus entry.

Amino Acid Sequence↗
PubMed1983

Plaque morphology and pathogenicity for newborn mice of swine vesicular disease virus. II. Temperature-dependent mutants and their clones.

From wild swine vesicular disease virus (SVDV) strains temperature-dependent (td) mutants td 27 degrees C, td 32 degrees C and td 42 degrees C were derived. Differences were noted in their pathogenicity for newborn mice. The non-homogeneity of the td populations was manifested by formation of plaques of various sizes and confirmed by differential pathogenicity of the clones derived from them. A higher pathogenicity of the td mutants and their clones was associated not only with larger plaques, but also with higher temperature permissive for the given mutant. The td 27 degrees C mutants were not virulent for newborn mice, similarly to the attenuated SVDV strain and its clones.

Animals↗
PubMed1997

Association of tumour necrosis factor and acute phase reactant changes with post arrival disease in swine.

Severe weight loss in the absence of respiratory, enteric or systemic clinical disease or gross pathologic lesions is often observed when immunologically naive boars are placed in conventional health swine facilities. Affected animals develop this weight loss in spite of receiving pre-entry vaccinations against common swine pathogens, such as Haemophilus parasuis or Mycoplasma hyopneumoniae. In many cases, the weight loss is non-responsive to long term antibiotic therapy. In order to determine the relationships between the severity of post arrival weight loss and disease and its potential immunological or physiological indicators, tumour necrosis factor (TNF) and acute phase reactant levels were correlated with the clinical status in immunologically naive boars following their transfer to a conventional facility. Boars had higher TNF (P < 0.0001) and plasma protein (P = 0.0054) levels and decreased zinc (P = 0.0004) levels during periods of clinical sickness. Likewise, peak and average plasma TNF, serum haptoglobin, and serum zinc were correlated indicating a prolonged stress or pathogenic insult (r = 0.89, P < 0.0001 for TNF; r = 0.67, P = 0.01 for haptoglobin; r = 0.73, P = 0.005 for zinc). An acute phase response, a systemic TNF increase and the development of a lymphopenia were observed in post arrival disease in swine. This is the first time cytokines and acute phase reactants have been investigated in a field study involving immunologically naive or high health swine.

Acute-Phase Proteins↗