Swine dysentery: protection of pigs by oral and parenteral immunisation with attenuated Treponema hyodysenteriae.

An attenuated strain of Treponema hyodysenteriae was used to immunise 18 pigs in three experiments. Live attenuated spirochaetes were dosed orally and injected intra-peritoneally, and killed spirochaetes were injected intramuscularly with adjuvant. The vaccinated pigs, which developed high serum agglutination titres against T hyodysenteriae, and 18 unvaccinated litter-mates were repeatedly challenged with virulent T hyodysenteriae. Nine vaccinated pigs and 16 control pigs developed typical swine dysentery.     

Effects of Long-term Cyanide Ingestion by Pigs

Animal performance and health status are adversely affected by long-term cyanide ingestion; however, the effects of cyanide ingestion by pigs have not been fully determined. The aim of the present study was to determine the effects of prolonged exposure to different doses of potassium cyanide (KCN) in growing-finishing swine. Twenty-four pigs, 45 days of age, were divided into four equal groups and treated with different doses of KCN: 0, 2.0, 4.0 or 6.0 mg per kg body weight per day for 70 consecutive days. The results showed a significant alteration in thiocyanate, creatinine and urea levels and in alanine aminotransferase activity of swine dosed with 4.0 and 6.0 mg/kg/KCN. Thyroid weight was significantly increased in those pigs from 4.0 mg/kg KCN group, but no change in cholesterol, triiodothyronine or thyroline levels were observed. Body and carcase weights, body weight gain, and bacon thickness were not affected by KCN treatment. The histopathological study revealed increased numbers of vacuoles in the colloid of thyroid follicles, degeneration of cerebellar white matter and Purkinje cells, degeneration of renal tubular epithelial cells, caryolysis and pyknosis in hepatocytes, and disturbance of the normal lobular architecture of the liver in all treated pigs. Thus, long-term administration of KCN to swine affects several tissues and could adversely affect animal production.     

Inhalation anesthesia induced by isoflurane alters penicillin disposition in swine tissues

Twelve healthy swine were dosed with penicillin G intramuscularly. Fluids and tissues samples were collected at the end of two periods of general anesthesia, performed 24 h apart. Tissue samples were collected by minimally invasive laparoscopy under general anesthesia at 8 and 28 h postdose. Four nonanesthetized, penicillin‐treated pigs were euthanized at 8 h postdose, and a second set of four similarly treated control pigs were sacrificed 28 h postdose. Liver penicillin tissue concentrations from animals that underwent anesthesia and laparoscopic tissue collection had tissue concentrations that were higher than nonanesthetized pigs at both time points. Urine, plasma, kidney, skeletal, and cardiac muscle showed no differences between the two groups. Laparoscopic tissue collection under general anesthesia in swine induces physiological changes that cause alterations in tissue pharmacokinetics not seen in conscious animals.     

Myocardial and pancreatic lesions induced by T-2 toxin, a trichothecene mycotoxin, in swine

Myocardial and pancreatic lesions induced by sublethal doses of T-2 toxin in swine were characterized by light and electron microscopy. Toxin was given intravenously to six 17- to 18-week-old pigs. Pigs were killed 24 or 48 hours after treatment. Grossly, subendocardial hemorrhages, multifocal pinpoint white foci in myocardium, and pancreatic edema occurred in one treated pig. Histologic changes in myocardium of treated pigs consisted of multifocal edema, mononuclear cell infiltration, myofiber hyalinization, vacuolation, and contraction bands with nuclear pyknosis. Ultrastructurally, there were areas of edema, myofibrillar disorganization, dilation of sarcoplasmic reticulum, and formation of hypercontraction bands. Myocardial mineralization was seen in the pig with gross lesions. Pancreatic changes in treated pigs consisted of multifocal acinar degeneration and necrosis. Ultrastructural changes included irregular dilation of rough endoplasmic reticulum and abnormal zymogen granules. Thus, in addition to radiomimetic lesions of the gastrointestinal tract and lymphoid organs, heart and pancreas are target organs of T-2 toxin in swine.     

Pathogenicity of an attenuated strain of transmissible gastroenteritis virus for newborn pigs.

The pathogenicity of a cell culture-attenuated strain of transmissible gastroenteritis virus for newborn pigs was investigated. Newborn (1- to 2-day-old) pigs were orally given 2 x 10(6) plaque-forming units of attenuated virus. All pigs developed mild diarrhea, but deaths did not occur. As determined by immunofluorescence and villous atropy, infection of the small intestine was limited to the caudal 50 to 66%. Fluorescing cells and atrophic villi were seen from 2 to 3 days until 6 to 7 days after exposure. Attenuated virus-exposed pigs produced circulating virus-neutralizing antibodies detectable as early as 5 days after exposure. By contrast, all pigs orally given 1 x 10(2) pig infective doses of virulent transmissible gastroenteritis virus developed severe diarrhea, and almost all of those not killed died within 2 to 5 days after exposure. In the latter pigs, the entire length of the small intestine, except for the first 4 to 5 cm, was infected with virus by 24 to 36 hours after exposure.     

Curing experimental Bryophyllum tubiflorum poisoning of cattle with activated carbon, electrolyte replacement solution and antiarrhythmic drugs

A slurry of activated carbon (activated charcoal) in electrolyte replacement solution given by stomach tube and antiarrhythmic drugs given parenterally cured 9 of 11 calves dosed 7 to 24 h previously with a lethal amount (20g/kg) of Bryophyllum tubiflorum flower heads. Two of another 4 calves treated 26 to 36 h after dosing with flowers survived. B. tubiflorum toxins are bufadienolides (cardiac glycosides). Activated carbon was effective at a single dose of 5 g/kg. Calves were rehydrated with oral electrolyte replacement solution at 150 ml/kg in divided doses over 24 h. Tachycardia was treated with intravenous lignocaine (200 mg doses) or propranolol (5 mg doses) and atrioventricular block with atropine (0.5 mg/kg).     

ENCEPHALOMYOCARDITIS VIRUS INFECTION OF PIGS 2. Experimental Disease

Encephalomycarditis virus recovered from a pig mortality in New South Wales was used to produce experimental infections. Of 34 pigs exposed, 17 died and a further 7 were found to have severe heart lesions when killed. Deaths occurred from 2 to 11 days after exposure with a mode of approximately 3 days. Ten of 11 pigs exposed by intramuscular injection died and the remaining pig was killed after 28 days and found to have severe resolving heart lesions. Of 15 pigs exposed per os to various doses of virus, 6 died, 4 were killed and found to have severe heart lesions and 5 were apparently not infected. Intranasal exposure of 8 pigs resulted in 1 death and 4 pigs with mild to severe heart lesions. Different doses of virus and routes of exposure did not substantially influence the character of the lesions. Lesions were similar to those found previously in field cases, and virus was recovered from all of 19 animals examined with severe acute lesions of 10 days standing or less.     

Experimentally induced Mycobacterium avium serotype 8 infection in swine.

Five of 6 swine experimentally inoculated with Mycobacterium avium serotype 8 had microgranulomas in the cervical or mesenteric lymph nodes at necropsy 92 days later. In vivo tuberculin skin reactivity and in vitro lymphocyte immunostimulation responses were evaluated at 10 and 12 weeks after the pigs were inoculated. Positive responses were obtained on both tests in inoculated pigs, whereas test results in noninoculated pigs and pigs given killed bacterial cells were negative. Mycobacterium avium serotype 8 was isolated at necropsy from the cervical or mesenteric lymph nodes of each of the pigs inoculated with viable microorganisms and from the 2 pigs kept in the pen with inoculated swine. Mycobacteria were not isolated from tissues of the noninoculated swine or those given killed cells.     

Protective immunity to Ascaris suum: analysis of swine peripheral blood cell subsets using monoclonal antibodies and flow cytometry

Outbred domestic swine or SLA inbred miniature swine were exposed to Ascaris suum either naturally on contaminated lots or by inoculation with UV-irradiated attenuated eggs. Both inbred and outbred swine developed virtually complete protection to a challenge of 10 000 eggs after natural exposure, but inbred swine were less resistant than outbred swine after UV-egg exposure. Flow cytometric analysis of peripheral blood mononuclear cells from these animals, performed to determine changes in cell subsets including helper T-cells, cytotoxic/suppressor T-cells, macrophages, and cells expressing class II major histocompatibility antigens, showed that both outbred and inbred swine had similar responses after parasite exposure. The levels of helper T-cells and cytotoxic/suppressor T-cells did not change after parasite exposure, while there was an appreciable but transient increase in macrophages only in those swine naturally exposed to A. suum. Swine exposed to A. suum, both naturally and by inoculation with UV-eggs, showed an increase in the amount of class II antigens detectable per cell. In a second set of experiments, outbred swine were exposed to A. suum naturally or by repeated experimental inoculation with different doses of normal eggs, and protective immunity and changes in blood cell subsets were determined. The greatest change in blood cell subsets was found at 3 and 5 weeks after initial parasite exposure, when macrophages were elevated moderately in a group of pigs inoculated every other day with 1000 eggs and markedly in a group that was naturally exposed; class II antigen expression was also increased during this period. These increases preceded peak serum antibody responses, which were lower in the naturally-exposed group relative to the experimentally-inoculated group. Both groups had high levels of protective immunity. This suggests than natural exposure to A. suum may activate cells and enhance specific immune responses to give high levels of protection.     

Immunity to Lancefield's group E Streptococcus: passive protection of swine

Healthy swine from one source were randomly allotted to 3 groups of 3 pigs each. Troup I and II pigs were parenterally dosed with serum obtained from swine in the convalescent stage of streptococcic lymphadenitis of swine. Group III pigs were contact controls. The swine of all groups were orally exposed to Lancefield's group E Streptococcus sp. During the next 3 weeks, the controls evidenced little resistance to the development of streptococcic lymphadenitis of swine, whereas the principals evidenced considerable resistance to development of the disease.     

Turbinate atrophy in gnotobiotic pigs intranasally inoculated with protein toxin isolated from type D Pasteurella multocida

Three doses (75 micrograms, 25 micrograms, and 25 micrograms) of purified toxin isolated from a toxigenic strain of type D Pasteurella multocida were given (by atomizer) into the right nasal cavities of each of 10 gnotobiotic pigs on the 21st, 24th, and 27th days of age, respectively. Inoculated pigs (usually 2) and 1 noninoculated control pig each were necropsied on 3, 6, 9, 12, and 15 days after inoculations were given. Severe bilateral atrophy of turbinates occurred in all toxin challenge-exposed pigs. Atrophy was more severe in the inoculated nasal cavity than that in the noninoculated side in 2 of the 10 pigs. Microscopic changes in turbinates of toxin challenge-exposed pigs were more severe in pigs killed at later dates. Dominant changes included degeneration and necrosis of osteoblasts, markedly accelerated osteoclastic osteolysis, replacement of the osseous core by a highly cellular mesenchymal stroma, and multifocal atrophy of submucosal glands. Seemingly, a protein toxin isolated from toxigenic type D strains of P multocida produced rapid atrophy of turbinates and may be a contributing factor in development of clinical progressive atrophic rhinitis in swine.     

Nephrotoxicity in Goats Caused by Dosing with a Water Extract from the Stems of Narthecium Ossifragum Plants

Seven goats were given a single dose of an aqueous extract derived from 30 g (wet weight) of Narthecium ossifragum per kg liveweight. Their serum creatinine and urea concentrations increased to day 5 but then fell to normal by day 10. Serum magnesium increased to day 4 and decreased to normal by day 9. Their serum calcium concentration was lower than normal on days 4, 5 and 6. Histopathological examination of the kidneys of goats killed or found dead 2, 4, 6, 8, 11 or 16 days after dosing revealed tubular epithelial cell degeneration and necrosis. Regeneration of the tubular epithelium and signs of interstitial fibroplast proliferation and fibrosis could be seen in animals killed on days 8, 11, 16 and 42. No signs of liver damage were observed in 3 goats dosed with the insoluble plant material from 40 g (wet weight) Narthecium ossifragum per kg liveweight. The total dose was divided into three doses, which were given intraruminally within 7 h. The activities of aspartate aminotransferase, -glutamyl-transferase and glutamate dehydrogenase remained within the normal range in all 10 goats after dosing.     

Effect of acute oral doses of T-2 toxin on tissue concentrations of biogenic amines in the rat

T-2 toxin [3 alpha-hydroxy-4 beta, 15-diacetoxy-8 alpha-(3-methylbutyryloxy)-12,13-epoxytrichotec-9-ene] is an emetic Fusarium trichothecene mycotoxin known to cause lethargy, ataxia and feed refusal in economically important animals. Experiments were conducted to determine the effect of acute oral doses of T-2 toxin on tissue concentrations of neurotransmitters thought to play some role in regulation of feed consumption. Sixty-seven male weanling rats were intubated with a few grams of diet in a liquid slurry with or without 2.0 mg T-2 toxin per kilogram of body weight. At 1, 2, 4, 6, 8, 12, 24 and 48 h following dosing, rats were killed, and brains, spleens, hearts and adrenal glands were excised and analyzed for concentrations of neurotransmitters and metabolites using high-performance liquid chromatography with electrochemical detection. Administration of T-2 toxin caused increases in brain concentrations of tryptophan and serotonin at the early time intervals after dosing. Brain concentrations of dopamine increased, whereas concentrations of 3,4-dihydroxyphenylacetic acid (DOPAC) decreased at the later time interals following dosing. Concentrations of dopamine were increased in adrenal glands, whereas epinephrine concentrations decreased. Epinephrine was detected in spleen and heart after administration of T-2 toxin. It was concluded that the increase in brain indoleamines induced by T-2 toxin could contribute to feed refusal in animals suffering from T-2 toxicosis.     

Effects of DNA dose,route of vaccination,and coadministration of porcine interleukin-6 DNA on results of DNA vaccination against influenza virus infection in pigs

OBJECTIVE: To examine the effects of DNA dose, site of vaccination, and coadministration of a cytokine DNA adjuvant on efficacy of H1-subtype swine influenza virus hemagglutinin (HA) DNA vaccination of pigs. ANIMALS: 24 eight-week-old mixed-breed pigs. PROCEDURE: 2 doses of DNA were administered 27 days apart by use of a particle-mediated delivery system (gene gun). Different doses of HA DNA and different sites of DNA administration (skin, tongue) were studied, as was coadministration of porcine interleukin-6 (pIL-6) DNA as an adjuvant. Concentrations of virus-specific serum and nasal mucosal antibodies were measured throughout the experiment, and protective immunity was assessed after intranasal challenge with homologous H1N1 swine influenza virus. RESULTS: Increasing the dose of HA DNA, but not coadministration of pIL6 DNA, significantly enhanced virus-specific serum antibody responses. Pigs that received DNA on the ventral surface of the tongue stopped shedding virus 1 day sooner than pigs vaccinated in the skin of the ventral portion of the abdomen, but none of the vaccinated pigs developed detectable virus-specific antibodies in nasal secretions prior to challenge, nor were they protected from challenge exposure. Vaccinated pigs developed high virus-specific antibody concentrations after exposure to the challenge virus. CONCLUSIONS AND CLINICAL RELEVANCE: Co-administration of pIL-6 DNA did not significantly enhance immune responses to HA DNA vaccination or protection from challenge exposure. However, HA DNA vaccination of pigs, with or without coadministration of pIL-6 DNA, induced strong priming of the humoral immune system.     

Sympathoadrenal Neurochemistry and early weaning of swine.

Three litters of pigs were weaned at 21 days of age, and 3 others were left with the sow. Pigs were killed at 21, 23, 28, or 39 days of age. Weaned pigs exhibited anxiety, gastrointestinal dysfunction, and decreased rate of body weight gain. Plasma glucose or liver glycogen concentrations were not decreased by weaning. Adrenal gland weights and tyrosine hydroxylase (EC 1.14.3a), dopamine beta-hydroxylase (EC 1.14.2.1), phenethanolamine-N-methyl transferase (EC 2.1.1), and monoamine oxidase (EC 1.4.3.4) activities were increased after weaning. Adrenal catecholamine and cortisol levels and dopa decarboxylase (EC 4.1.1.26) and catechol-o-methyl transferase (EC 2.1.1.6) activities were not significantly altered, although some increases were indicated. Cranial cervical ganglionic choline acetyltransferase (EC 2.3.1.6) and tyrosine hydroxylase activities were increased after weaning. Weaning of swine at 21 days of age is a stressful experience, and many effects persist for at least 18 days; however, growth was no longer impaired 18 days after weaning.     

Monensin toxicosis in swine: potentiation by tiamulin administration and ameliorative effect of treatment with selenium and/or vitamin E

Modulation of acute monensin toxicosis in swine was evaluated in 2 studies. In study 1, 56 weanling male pigs were allotted to 14 groups of 4 each. Pigs in 7 groups were given tiamulin in the drinking water (to supply 7.7 mg/kg of body weight/day) for 3 days before and for 2 days after monensin administration. Monensin was given as a single oral dose (at 0, 7.5, 15, 25, 50, 75, or 100 mg/kg) to pigs in groups with or without tiamulin exposure. Prominent acute clinical signs of monensin toxicosis (hypermetria, hind limb ataxia, paresis, knuckling of hind limbs, and recumbency) developed by 2 to 6 hours after dosing in pigs given 15 or 25 mg of monensin/kg with tiamulin exposure, but not in pigs given the 15 or 25 mg of monensin/kg without tiamulin exposure. Also, the extent of monensin-induced skeletal muscle damage at 4 days after monensin dosing was enhanced in pigs given 7.5, 15, or 25 mg of monensin/kg and exposed to tiamulin. In study 2, 48 weanling male pigs were allotted to 8 groups of 6 each. Four groups of pigs were given 20 mg of monensin/kg orally, and 4 groups were given 100 mg of monensin/kg orally. For each monensin dose, a group was treated 24 hours before monensin administration with (i) selenium (Se)-vitamin E preparation, 0.25 mg of Se and 68 IU of d-alpha-tocopheryl acetate (vitamin E)/kg, IM; (ii) vitamin E only, 68 IU of d-alpha-tocopheryl acetate/kg; (iii) Se only, 0.25 mg of Se/kg; or (iv) vehicle.(ABSTRACT TRUNCATED AT 250 WORDS)     

Preliminary study of the pharmacokinetics and toxicopathy of deoxynivalenol (vomitoxin) in swine

Study was made of the pharmacokinetics and toxicopathy of deoxynivalenol (DON, vomitoxin) given IV to swine. In the 24 hours after swine were given DON, clinical signs of vomiting, diarrhea, muscular weakness, tremors, and twilight coma were similar to those observed with other 12,13-epoxytrichothecenes. Hypoglycemia and pancreatic islet cell lesions were observed which indicated that DON-induced changes in intermediary metabolism may be an insidious aspect of DON intoxication. Histopathologic examination of all organ systems revealed pancreatic acinar and islet cell necrosis and mild lympholysis of the mesenteric lymph nodes. The renal excretion of DON was altered by IV infusion of saline solution. Pharmacokinetic findings may indicate that DON was both secreted and reabsorbed by the renal tubules. The half-life of DON ranged from 2.08 to 3.65 hours. Residues of DON were not found in skeletal muscle of swine at 24 hours after dosing.     

Immune responses in swine given lipid-conjugated pseudorabies viral antigens.

The immune response was compared in pigs given inactivated pseudorabies virus (PRV) antigens (with or without adjuvant) or PRV antigens covalently conjugated with a fatty acid (lauric acid) to enhance delayed-type hypersensitivity. The pigs were given 2 inoculations, 14 days apart, and were challenge exposed 28 days after the 1st inoculation. Pibs inoculated with PRV antigens, with or without adjuvant, had significant virus-neutralizing (VN) antibodies before challenge exposure, but the pigs inoculated with lipid-conjugated PRV antigens had no detectable VN antibodies, with the exception of 1 pig. All inoculated pigs were positive by the microimmunodiffusion test at postinoculation day 14 and remained positive throughout the experiment. The inoculated pigs had delayed-type hypersensitivity reactions when skin tested a postinoculation day 25; the pigs inoculated with lipid-conjugated PRV antigens had a more pronounced reaction. Inoculated pigs had mild respiratory signs on the 3rd through the 6th days after challange exposure, with no observable difference in severity between the inoculated groups. The control pigs had acute signs of PRV, and 3 or 4 pigs died 5 to 8 days after challenge exposure. The average VN titers of the different inoculated groups of pigs were nearly equal 2 weeks after challenge exposure. Results indicated that both humoral antibodies and cell-mediated immunity have a role in PRV infections in swine.     

Relative bioactivity of dietary RRR- and all-rac-alpha-tocopheryl acetates in swine assessed with deuterium-labeled vitamin E

This study evaluated the relative bioactivities of natural and synthetic stereoisomers of alpha-tocopherol in swine. Deuterium-labeled vitamin E (150 mg each of d3-RRR- [natural] and d6-all-rac- [synthetic] alpha-tocopheryl acetates) was administered orally to adult female pigs (n = 3) with the morning feed. Blood samples were obtained at 0, 3, 6, 9, 12, 36, 48, and 72 h after the dose. The time of maximum plasma d3-alpha-tocopherol concentration (0.486 microg/mL) occurred at 12 h, and d6-alpha-tocopherol peaked earlier (at 9 h) and at a lower (P < 0.05) concentration (0.288 microg/mL). The d3-/d6-alpha-tocopherol ratio increased from 1.35 (SD = 0.73) at 3 h after dosing to 2.0 (SD = 0.14) at 72 h (P = 0.03). The plasma disappearance rates of d3- and d6-alpha-tocopherols (post-maximum concentrations) were similar and were estimated to be 0.013 microg/mL per hour. In summary, swine discriminated between RRR- and all-rac-alpha-tocopherols, which resulted in an approximately twofold higher plasma alpha-tocopherol concentration arising from the RRR-form. This 2:1 ratio of RRR- to all-rac- is higher than the currently accepted USP definition of RRR-:all-rac- of 1.36:1.00.     

Urinary excretion of immunoreactive sporidesmin metabolites in sheep in relation to factors influencing susceptibility to sporidesmin intoxication

AIM: To study the urinary disposition of orally administered sporidesmins A and D in sheep and identify factors influencing their kinetics, particularly the influence of breeding for resistance and susceptibility to sporidesmin, the mycotoxin responsible for the hepatogenous photosensitisation, facial eczema. METHODS: A competitive ELISA was used to monitor urinary output of immunoreactive metabolites after the intraruminal administration, to female Romney sheep, of either sporidesmin A or sporidesmin D, the nontoxic analogue. Preliminary characterisation of metabolites was carried out using HPLC with fractions monitored by ELISA. RESULTS: Maximum urinary excretion rates of immunoreactive metabolites occurred 2-8 h after dosing with sporidesmin D and 15-30 h after dosing with sporidesmin A. Sporidesmin D caused no liver injury, as detected by changes in serum enzyme activity, while the liver injury caused by sporidesmin A was greatest for the sheep with the highest cumulative output of metabolite. When sporidesmin D was administered in two separate doses to sheep bred for either resistance or susceptibility to facial eczema, the variability of metabolic output between sheep within groups was much less after the second dose. The mean urinary metabolite excretion was greater for the susceptible than the resistant sheep but the difference was not significant. Potentiation (caused by pre-administration of small doses of sporidesmin A) resulted in a more severe reaction to the dosed sporidesmin A. Urinary output of metabolite was less in the potentiated than in the unpotentiated sheep. When resistant and susceptible sheep were dosed with sporidesmin A after potentiation there was no difference between them in their cumulative totals or excretion rates of immunoreactive metabolites. However, the volume of urine produced by the susceptible sheep was lower and less variable than the resistant sheep and consequently the concentration of their urinary metabolites was higher. Preliminary ELISA examination of HPLC-fractionated urine from a sheep dosed with sporidesmin A indicated the presence of several metabolites of sporidesmin. CONCLUSION: Sporidesmin A and metabolites are rapidly excreted in urine but not as rapidly as sporidesmin D and its metabolites. Only minor differences between sheep bred for resistance and susceptibility were seen. Potentiation caused a more severe reaction to sporidesmin A and less urinary excretion of the sporidesmin and its metabolites. CLINICAL RELEVANCE: This work is part of a programme with the aim of identifying FE-resistant animals without the need for sporidesmin dosing.