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Biomedical subjects

I W Wilkie

Publications and source records attributed to I W Wilkie.

11 recordsLinked to original sources
PubMed2000

The demonstration of Pasteurella multocida in the alimentary tract of chickens after experimental oral infection.

A selective medium containing polymyxin B, crystal violet, thallous acetate, bacitracin and cycloheximide in 10% sheep blood dextrose starch agar, and a modified Pasteurella multocida-specific polymerase chain reaction (PCR) assay were developed for the respective isolation and detection of P. multocida from chicken alimentary tract. The selective medium and the PCR assay were highly sensitive, detecting 100 cfu from colon contents. These techniques were used to follow the localisation of an orally administered virulent P. multocida in chickens. Pasteurellae could be isolated from the crop of some birds up to 30 h, occasionally from other sites after 28 h. It was concluded that the crop was a likely site for colonisation and that infection was most likely to occur through the mucosa of the jejunum or ileum.

Administration, Oral↗
PubMed2000

The virulence and protective efficacy for chickens of pasteurella multocida administered by different routes.

The relative virulence for chickens of five strains of Pasteurella multocida was evaluated. Twenty groups, each of ten chickens, were inoculated with a standard dose of 10(5) of each of five strains by the intramuscular (I.m.), intravenous (I.v.), intratracheal (I.tr.) or conjunctival (Co) routes. The highest mortality occurred in the groups dosed I.m. and I.v., followed by I.tr. inoculation. The relative virulence of each strain did not change when inoculated by the different routes. The most virulent strain, VP161, caused 100% mortality by all except the Co route. The least virulent strain, VP17, caused a single mortality by the I.v. route, but gave a high level of protection to birds inoculated by both the I.m. and I.v. routes, when challenged by intramuscular injection with (VP161). There was no protection against I.m. challenge in the birds inoculated by the I.tr. or Co routes. Serum antibody levels measured by ELISA correlated with the level of protection against virulent challenge for groups inoculated I.m. or I.v., but not I.tr. Western blots of pooled sera from each group did not show any specific antigen recognition that might explain the observed differences in protection. Inoculation with strain VP17, (both I.m. and I.tr.) also gave a high level of protection to birds challenged with strain VP161 by intratracheal instillation.

Animals↗
PubMed1990

The effect of Pasteurella haemolytica and the leukotoxin of Pasteurella haemolytica on bovine lung explants.

Bovine lung explants were used in a study designed to compare the pathogenic effects of Pasteurella haemolytica type 1, a nonpathogenic organism Neisseria subflava, or the crude leukotoxin of P. haemolytica on alveolar macrophages and lung parenchymal cells. Concentrated, purified peripheral blood neutrophil suspensions were added with the bacteria to some explants. Duplicate pairs of cultures from each treatment group were fixed at regular intervals up to 24 hours after seeding and morphological changes were assessed by light and electron microscopy. Pasteurella haemolytica caused deterioration of alveolar macrophages within one hour but did not affect parenchymal cells for more than 12 hours. Neisseria subflava did not affect alveolar macrophages initially, but caused an accelerated deterioration after four hours. After 24 hours, bacterial overgrowth caused similar deterioration of all cells in explants seeded with either bacterium. Alveolar macrophages phagocytosed large numbers of N. subflava but rarely ingested P. haemolytica. Added neutrophils did not have any discernible effect on any of the explants and did not potentiate bacterial effects. Addition of crude leukotoxin of P. haemolytica to the culture medium significantly accelerated alveolar macrophage deterioration without apparent effect on parenchymal cell survival. These results support the hypothesis that the severe tissue destruction of fulminant pneumonic pasteurellosis is not a direct result of bacterial infection.

Animals↗
PubMed1985

The hepatotoxicity of carbon disulphide in sheep.

Carbon Disulphide (CS2) caused liver injury when dosed orally (intraruminally) at 0.05 ml per kg body weight to overnight fasted sheep which had been given 200 mg kg-1 DDT intraruminally 1 week previously to enhance the hepatic mixed function oxygenases. The liver lesion was a periacinar hepatocellular vacuolar degeneration, fully developed at 24 h and lasting from 4 to 5 days after which the hepatic morphology returned to normal. At 24 h after dosing with CS2 there was an increase in total liver water, sodium and potassium ions but without an increase in the concentration of these cations in total liver water, and a 50% reduction in microsomal cytochrome P450 levels. Calcium concentration was either unchanged or only slightly increased. The cytoplasmic vacuoles were mainly distensions of the rough endoplasmic reticulum and contained fine amorphous or fibrillary material, probably originating from damaged smooth endoplasmic reticulum membranes. The transient influx of fluid into these organelles is thought to be due to osmotic action generated by molecules derived from the latter macromolecular membrane fragments. The lesion resembles that seen in the rat due to CS2 after pretreatment with phenobarbitone. In situations in which sheep are drenched with CS2 and CCl4 in combination, it is suggested that the development of hepatic periacinar hydropic change due to the CS2 in animals normally susceptible to CCl4 because of enhanced microsomal cytochrome P450 levels would provide a better chance of survival than if CCl4 alone was administered and extensive periacinar coagulative necrosis occurred.

Animals↗
PubMed1982

Estimation of antemortem serum electrolytes and urea concentrations from vitreous humor collected postmortem.

Electrolyte and urea levels of vitreous humor collected from bovine eyes at various times postmortem, were compared with serum levels in the same animals. Provided the vitreous humor was filtered immediately after collection, measured levels of total calcium (Ca), potassium ions (K+), sodium ions (Na+) and urea nitrogen were very consistent. For 24 hours postmortem the concentrations of Ca, Na+ and urea nitrogen remained stable, while K+ increased to approximately 55% more than the immediate postmortem level. A small study using anesthetized dogs indicated that urea nitrogen levels of vitreous humor take several hours to equilibrate with elevated blood levels. Analysis of vitreous humor may be a useful adjunct to diagnosis in cases where antemortem clinical chemistry is absent or inadequate.

Abattoirs↗
PubMed1981

Influence of weed seed oil contamination on the nutritional quality of diets containing low erucic acid rapeseed (Brassica napus, Tower cultivar) oil when fed to rats.

Oils from three samples of rapeseed screenings and a sample of stinkweed seeds (Thlaspi arvense) were added to Tower rapeseed oil at three levels (5, 10 and 15%). The contaminated Tower oils were fed at 20% (w/w) of a purified diet to male weanling Sprague-Dawley rats for 16 weeks. The screenings oils caused no increase in the focal myocardial lesion index or lipidosis of the rat hearts. Stinkweed oil gave a significant increase in myocardial lipidosis and a non-significant increase of the myocarditis index. These were attributed to an imbalance in the fatty acid composition of the Tower oil for the specific requirements of the growing rat. Screenings oil contamination had no significant effects on the feed intake or growth of the animals. The growth of rats fed stinkweed oil-contaminated diets was significantly lower than other treatments when it was adjusted for feed intake by analysis of covariance. No treatment effects on body organ weights nor on blood lipid parameter were observed. The presence of week seed oils, at the highest levels likely to be encountered in low erucic acid rapeseed oil, was concluded to have a significant influence on its nutritional value.

Animals↗
PubMed1981

Polyserositis and meningitis associated with Escherichia coli infection in piglets.

Two piglets which had a history of anorexia and weakness were examined pre and postmortem. Other piglets in the same herd had died within 24 hours of the onset of similar signs. The two piglets examined had a fibrinous polyserositis. Grossly, the pleura, peritoneum and joints were affected and an acute meningitis was noted on microscopic examination of the brains. Pure cultures of Escherichia coli were recovered from all but one of the organs and exudates cultured.

Animals↗
PubMed1980

Leukomyelitis in the goat: a report of three cases.

Three cases of focal myelitis in the spinal cords of young goats are described. The clinical findings and pathological changes were similar to those reported for viral leukoencephalomyelitis of goats. There were granular structures in a few cells in malacic areas, which on electron micrographs appear to be clumps of chromatin in the nuclei of gemistocytic astrocytes. They may represent mitotic figures.

Animals↗