RESPIRATORY DISEASES OF SWINE.
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Swine vesicular disease (SVD) caused problems in 1993 when it was detected in Dutch pigs in Italy. As a result, the EC took measures against the export of live pigs. In all cases the animals had been retained at an Italian abattoir or farm for three days or more, which is longer than the minimum incubation time. Extensive clinical inspections and serological testing on the farms from where the pigs originated revealed no evidence of SVD infection. Serological testing for SVD of over 1.5 million blood samples collected from herds within the framework of export- and herd certification, and the testing of slaughter sows and slaughter boars (EC directive), was negative as well. In view of these results it has to be assumed that the Dutch pig population is free from SVD and that the pigs were infected in Italy. However, a complaint from Italy in 1994 led to the detection of two SVD virus-contaminated export collection centres. If the existing regulations on the cleansing and disinfection of the transport chains are stringently enforced and implementation of the rules is continuously supervised, then it may be expected that the problems have been overcome.
The antigenic region of VP1 gene of swine vesicular disease virus was amplified by reverse transcription polymerase chain reaction (RT-PCR) and nested polymerase chain reaction (nPCR). After the amplified fragment was cloned into the expression vector pProEX-HTb. The insert position,the size and the reading frame of the insertion were identified by PCR, restriction digestion and sequence analysis of the recombinant plasmids. SDS-PAGE and Western blot indicated that the transformed BL21(DE3) by the recombinant plasmids and induced by IPTG could express the antigen region of VP1 of swine vesicular disease virus, the expressed antigen protein could be recognized by the positive serum of SVDV.
Tulathromycin, a novel triamilide antimicrobial, was evaluated for treatment of swine respiratory disease (SRD) in field efficacy studies involving 720 pigs in six North American swine herds. In each study, feeder pigs with clinical SRD were randomly assigned in equal numbers to a group treated with tulathromycin given as a single injection at 2.5 mg/kg of body weight or to a saline-treated control group. Four of the studies included a third group treated with ceftiofur sodium for 3 consecutive days at 3 mg/kg of body weight. Pigs were treated on day 0 and evaluated for treatment response on day 7. In each study, 10 or more nontreated pigs and saline-treated pigs that did not respond to treatment underwent necropsies to obtain lung samples that were evaluated for SRD pathogens. The overall cure rate was 46.4% for saline-treated pigs, 71.1% for tulathromycin-treated pigs, and 63.1% for ceftiofur-treated pigs. The cure rate for tulathromycin-treated pigs was significantly higher than for saline-treated pigs (P = .0116). Mortality from SRD occurred in 24 control pigs, seven tulathromycin-treated pigs, and one ceftiofur-treated pig. The mortality rate was significantly lower for both the tulathromycin- and ceftiofur-treated pigs compared with those treated with saline (P = .0148 and P = .0195, respectively). Actinobacillus pleuropneumoniae, Pasteurella multocida, Haemophilus parasuis, and Mycoplasma hyopneumoniae, bacteria commonly associated with SRD, were isolated from SRD-affected pigs. Under field conditions, tulathromycin injectable solution given as a single IM dose of 2.5 mg/kg of body weight was safe and effective in the treatment of SRD.
Enteric bacterial infections are among the most common and economically significant diseases affecting swine production worldwide. Clinical signs of these infections include diarrhea, reduced growth rate, weight loss, and death of preweaned, weanling, grower-finisher, young and adult age breeding animals. The most common etiological agents include Escherichia coli, Clostridium perfringens, Lawsonia intracellularis, Salmonella enterica, and Brachyspira (Serpulina) spp. With the exception of Brachyspira (Serpulina) hyodysenteriae, the cause of swine dysentery, and Lawsonia intracellularis, the cause of proliferative enteropathy, the pathological changes seen with these agents closely resemble the diseases occurring in human beings. Histological changes in the intestines of swine with enteric bacterial infections include bacterial colonization without significant damage (e.g., certain enterotoxigenic E. coli and C. perfringens type A), attaching and effacing lesions with enteropathogenic E. coli and Brachyspira pilosicoli, the cause of colonic spirochetosis, inflammation with S. enterica, and necrotizing and hemorrhagic lesions with certain C. perfringens. Extraintestinal spread of bacteria and/or toxins occurs with some serotypes of E. coli and most serotypes of S. enterica. Enteric bacterial diseases of swine have been used as models to study the pathogenesis of similar diseases of human beings. Several of these pathogens are also important causes of food-borne disease in humans.
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The article gives a comprehensive review on swine vesicular disease (SVD). The properties of the virus, symptoms, diagnosis, epizoötiology and control of the disease are described. The clinical appearance is illustrated by photographs from experimental infections. The differences in the epizoötiology of SVD and foot-and-mouth disease are discussed.
A real-time PCR assay based on primer-probe energy transfer (PriProET) was developed to detect swine vesicular disease virus (SVDV). Specificity tests of SVDV and heterologous virus showed specific amplification of SVDV strains only. The amplification plot for the closely related Coxsackievirus B5 remained negative. The sensitivity of assay was five copies of viral genome equivalents. A key point of the assay is tolerance toward mutations in the probe region. Melting curve analysis directly after PCR, with determination of probe melting point, confirmed specific hybridisation of the SVDV strains. Eight of twenty SVDV strains tested, revealed shifted melting points that indicated mutations in the probe region. All predicted mutations were confirmed by nucleotide sequencing. With the PriProET system there is a chance to identify phylogenetically divergent strains of SVDV, which may appear negative in other probe-based real-time PCR assays. At the same time, any difference in melting points may provide an indication of divergence in the probe region. The high sensitivity, specificity, and tolerance toward mutations in the probe region of the SVDV PriProET assay may improve the early and rapid detection of a wide range of SVDV strains, allowing reduced turnaround time and the use of high-throughput, automated technology.
Aujeszky's disease is caused by a herpesvirus. The pig is the natural host and sole source of dissemination of the virus. After a primary infection, during which the pig excretes virus for 10-14 days, the virus remains latent in the host. Eradication has been achieved in individual herds, areas and countries with a low prevalence. The crucial question is whether it is feasible to eradicate the virus in heavily infected areas. Using so-called marker vaccines in conjunction with companion diagnostic test kits the virus was eliminated in individual herds. The preliminary results of extensive field studies to investigate whether intensive vaccination curtails the circulation of virus are encouraging.
A Shiga-like toxin type II variant (SLT-IIv) is produced by strains of Escherichia coli responsible for edema disease of swine and is antigenically related to Shiga-like toxin type II (SLT-II) of enterohemorrhagic E. coli. However, SLT-IIv is only active against Vero cells, whereas SLT-II is active against both Vero and HeLa cells. The structural genes for SLT-IIv were cloned from E. coli S1191, and the nucleotide sequence was determined and compared with those of other members of the Shiga toxin family. The A subunit genes for SLT-IIv and SLT-II were highly homologous (94%), whereas the B subunit genes were less homologous (79%). The SLT-IIv genes were more distantly related (55 to 60% overall homology) to the genes for Shiga toxin of Shigella dysenteriae type 1 and the nearly identical Shiga-like toxin type I (SLT-I) of enterohemorrhagic E. coli. (These toxins are referred to together as Shiga toxin/SLT-I.) The A subunit of SLT-IIv, like those of other members of this toxin family, had regions of homology with the plant lectin ricin. SLT-IIv did not bind to galactose-alpha 1-4-galactose conjugated to bovine serum albumin, which is an analog of the eucaryotic cell receptor for Shiga toxin/SLT-I and SLT-II. These findings support the hypothesis that SLT-IIv binds to a different cellular receptor than do other members of the Shiga toxin family but has a similar mode of intracellular action. The organization of the SLT-IIv operon was similar to that of other members of the Shiga toxin family. Iron did not suppress SLT-IIv or SLT-II production, in contrast with its effect on Shiga toxin/SLT-I. Therefore, the regulation of synthesis of SLT-IIv and SLT-II differs from that of Shiga toxin/SLT-I.
The pathways of infection in swine vesicular disease have been studied by (i) an estimation of the amounts of virus required to produce infection by different artificial inoculation procedures; (ii) the distribution and amounts of virus in various tissues of pigs killed at intervals after contact infection; (iii) an investigation of the susceptibility to virus infection of pig tissue explants. The results show that pigs can be infected by a number of pathways and that the skin, as the most susceptible tissue, is probably the most frequent route of infection.
Purified suspensions of Coxsackie B5 virus and swine vesicular disease virus (SVDV) were prepared by harvesting and purifying cell pack virus. Crossed immunoelectrophoresis was carried out with purified N and H antigen fractions (full and empty particles). Relative migration velocity (RMV) was calculated for the N antigen fraction of 3 SVD viruses (UKG72, HK71 and Italy 66) and 2 Coxsackie B5 viruses (Faulkner and 8068). The prototype strain of Coxsackie B5 virus (Faulkner) had a low RMV almost identical to that of the first isolated strain of SVDV, Italy 66. A recent isolate of Coxsackie B5 virus (8068, isolated in UK in 1973) had a relatively high RMV very close to that of the UKG72 strain of SVDV isolated in the UK in 1972. Also the Hong Kong strain of SVDV (HK71) had a high RMV value. These observations are considered in relation to the emergence of swine vesicular disease.
A Brazilian stock of clone C17 of the IB-RS-2 porcine kidney cell line which was contaminated with hog cholera virus (HCV) was cloned. One clone designated IB-RS-2 D10 was determined to be free of HCV, 20 other viruses, and Mycoplasma. IB-RS-2 D10 cells possessed the same viral susceptibility pattern as the contaminated parent cells to the viruses of foot-and-mouth disease, swine vesicular disease, vesicular exanthema of swine, transmissible gastroenteritis, and several other viruses. The IB-RS-2 D10 cells had a median chromosome count of 34, were morphologically epithelioid cells, and were resistant to HCV infection. Freedom from HCV affords advantages for vaccine production and avoids laboratory contamination.
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Diseases and losses were registered in dependence on vitamin A supply with 2,035 pigs (6.5-114 kg live weight). The histologic examinations comprised various organs of 72 animals. The content of the main protein fractions as well as antibody titre after supplementing antigenes were determined in the serum of 104 animals. The feeding of a vitamin-A- and carotinefree casein-starch-respectively a Vitamin-A-free cereal-soybeanmeal-diet led to deficiency symptoms after 7-8 respectively 16-19 weeks of experiment particularly in the shape of nervous disturbances and voice affectations. Histologically a hyperplasia and a metaplasia of the epithelium of the big ducts in the salivory gland could be proved. The repletion of a part of the avitaminotic animals by means of oral (500 I.U./kg feed) and parenteral (500,000 to 1,000,000 I.U. i.m.) vitamin A administration is proof of a lack of vitamin A. Vitamin A and provitamin dosage did not influence diseases and losses with the exception of the occurrence of deficiency symptoms. The protein content of the serum as well as that of the globulin fractions alpha, beta, gamma did not change, the albumin content was lower in the groups without vitamin A (p greater than 0.05). Antibody titre against the lipopolysaccharide of salmonella dublin and human gamma globulin were diminished in piglets and fattening pigs fed vitamin A free (p less than 0.05). Taking the criterion of animal health, a vitamin A requirement higher than for growth (250 I.U./kg feed) cannot be derived.