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Biomedical subjects

C F Simpson

Publications and source records attributed to C F Simpson.

At least 37 records · Page 2Linked to original sources
PubMed1983

Acute experimentally induced aflatoxicosis in the weanling pony.

Nineteen weanling ponies and 1 adult pony were given a single oral dose of aflatoxin B1 (AFB1). Dosages were: 0, 0.5, 1, 2, 4, 5, 6, and 7.4 mg of AFB1/kg of body weight. Vital signs were monitored, and whole blood and serum collected for analysis of serum enzymes, prothrombin time, blood cell counts, and serum urea nitrogen. Ponies that died were examined for gross lesions, and tissues were collected for histopathologic examination and analysis of AFB1 and AFM1 residues. Two of the 4 ponies given the 2 mg/kg dose and all ponies given the larger dosages died within 76 hours. Clinical signs included increased rectal temperature, faster heart and respiratory rates, abdominal straining, bloody feces, and tetanic convulsions. At necropsy, ponies that died of acute aflatoxicosis showed visceral petechiae and hepatic focal lesions. Histopathologic changes included severe hepatic necrosis, vacuolation, and bile duct hyperplasia. Aflatoxins B1 and M1 were recovered from liver, kidney, skeletal muscle, and gastrointestinal contents. One other pony given the 2 mg/kg dose died 32 days after dosing, and 1 control pony died after 70 days. Continuous elevations in prothrombin time and serum aspartate aminotransferase, alanine aminotransferase, and gamma-glutamyl transpeptidase levels were observed in ponies dosed at 4 mg/kg or more. Significant (P less than 0.05) elevations in these values, which peaked 2 to 3 days after dosing, were seen in ponies given the 2 mg/kg dose. This group also had significant increases over controls in PCV and hemoglobin concentration 5 days after dosing.

Acute Disease↗
PubMed1983

Modification of the effects of aflatoxin B1 and warfarin in young pigs given selenium.

Selenium may be related to the hepatic metabolism of the coumarin compounds aflatoxin B1 and warfarin. Selenium evidently increased the pharmacologic activity of warfarin, probably due to a displacement of warfarin from albumin by selenium, the close relationship among selenium, vitamin E, and sulphur-containing groups (eg, glutathione), or the antioxidant effect of selenium. A diet containing selenium in a concentration of 2.5 mg/kg of feed was protective against the toxic effects of both coumarins in pigs given 4 daily oral doses of 0.2 mg/kg of body weight. Selenium, as glutathione peroxidase, at least in part, protects the hepatic cells against the toxic effects of aflatoxin B1 and warfarin. The protection was demonstrated by alteration of clinical responses and hematologic (prothrombin times), electrophoretic, and clinical chemistry values. It also was demonstrated that selenium at 2.5 mg/kg of feed does not produce toxic effects; however, dietary selenium at a concentration of 5 mg/kg (and in the presence of both toxic agents) was toxic for young pigs within the 3-week experimental period. Warfarin was more active as an anticoagulant than aflatoxin B1.

Aflatoxin B1↗
PubMed1982

Fate of microfilariae of Dirofilaria immitis following use of levamisole as a microfilaricide.

A pretreatment liver biopsy was secured from each of three dogs with Dirofilaria immitis microfilariae counts of 29,500, 24,700, and 76,700/ml blood, respectively. Post-treatment biopsies were obtained 30 h later following treatment with a single dose of levamisole and a reduction in microfilariae counts of up to 80%. Both pre- and posttreatment biopsies were examined by light and electron microscopy. Microfilariae in dilated sinusoids of pretreatment liver biopsies were not degenerated and were unattended by an inflammatory reaction when examined by either method. However, degenerated microfilariae were present within granulomas in post-treatment liver biopsies examined by light and electron microscopy. Several stages of degeneration of microfilariae, including phagocytosis, were identified by the latter method.

Animals↗
PubMed1982

Effect of hydralazine on aortic rupture induced by B-aminopropionitrile in turkeys.

The effects of hydralazine on aortic rupture, hemodynamics and aortic ultrastructure were studied in turkeys fed B-aminopropionitrile (BAPN). A mortality rate of 24% due to hemopericardium and internal hemorrhage in turkeys fed only BAPN increased to 91% when turkeys were fed both BAPN and hydralazine, despite a significant reduction in blood pressure after both drugs. Death rates among turkeys fed BAPN and hydralazine were lowered by adding either dietary propranolol (53%), which lowered blood pressure and dP/dt max, or reserpine (67%), which reduced blood pressure and increased dP/dt max. Striking ultrastructural alterations of collagenous and elastic fibers of the aortic media, which were additive to the effects of BAPN alone, were induced by BAPN and hydralazine. This study demonstrates that a 6-week feeding of high levels of BAPN and hydralazine, which accumulates in vessel walls, can produce vascular injury and increase mortality from hemorrhage in lathyritic turkeys.

Aminopropionitrile↗
PubMed1982

Vanadium metabolism in sheep. I. Comparative and acute toxicity of vanadium compounds in sheep.

Twelve Florida native wethers were given ammonium metavandate, calcium orthovanadate and calcium pyrovanadate by capsule in a study to examine the toxicity of the compounds. The initial daily dosage of 100 mg elemental vanadium was increased by 50 mg at 2-d intervals for an assessment not only of the toxic effects, but also to determined the amount that caused a decline in feed intake to 25% of that of control animals. The initial decline in feed intake was observed at 400 to 500 mg vanadium/d (9.6 to 12 mg/kg body weight, 310 to 350 ppm); a rapid decline in feed intake was accompanied by diarrhea. One sheep fed 550 mg vanadium as calcium orthovanadate died 3 d after dosing. One animal on each of the other three treatments was killed and necropsied for immediate comparison. Extensive mucosal hemorrhage of the small intestine and diffuse or petechial subcapsular hemorrhages of the kidneys were observed for sheep fed all compounds. The three vanadium compounds appeared to be similar in toxicity, as determined by abrupt declines in feed intake and pathological changes of the intestine and kidney. For a determination of acute toxicosis, three sheep were given 40 mg/kg body weight of vanadium as NH4VO3 in gelatin capsules and two sheep were included as controls. Two of the treated animals died within 80 h after administration and the other three were killed at 96 h. Vanadium content of kidney, liver, bone, spleen, lung and muscle was elevated by treatment.

Acute Disease↗
PubMed1982

Relationship of growth depression from salt deficiency and biotin intake to foot pad dermatitis of turkey poults.

Foot pad lesions in turkey poults were visually and microscopically examined in two experiments. Poults with normal growth had a high incidence of foot pad dermatitis. Histology of the foot pads indicated a biotin deficiency. Foot pad dermatitis was infrequent when growth was reduced as a result of lowered dietary salt intake. No histologic evidence of biotin deficiency was found in foot pads of poults fed a diet containing no supplemental salt.

Animals↗
PubMed1982

Influence of Protamone on fatty liver syndrome in commercial laying hens.

Two experiments were conducted to determine the influence of Protamone on fatty liver syndrome in commercial laying hens. The addition of either 110 or 220 mg of protamone per kilogram of diet significantly lowered liver fat and also significantly reduced body weight. From histological examination of livers of hens fed Protamone it was found that the hepatocytes contained little or no lipid, whereas hepatocytes of hens fed the control diet were turgid with lipid. The addition of Protamone to the diet resulted in a significant reduction in egg production without effecting feed efficiency in Experiment 1. In Experiment 2, egg production was significantly reduced and feed efficiency improved during Days 1 to 28. However, feed efficiency was poorer during Days 29 to 56 for hens receiving the Protamone.

Animals↗
PubMed1982

Toxicology of aflatoxin B1, warfarin, and cadmium in young pigs: metal residues and pathology.

The effects of feeding dietary cadmium (83 micrograms/g of diet) to young pigs on the distributions of copper, iron, and zinc in urine samples and in kidney, liver, and muscle tissues was determined. The diet with added Cd resulted in renal and hepatic tissue concentrations of 42.90 +/- 10.57 micrograms/g and 7.90 +/- 2.37 micrograms/g, respectively, at the 40th day of the experiment. Iron was found to decrease at the same time, which predisposed to the anemic condition of these pigs. The feeding of dietary CD to pigs prevented extensive fatty hepatocytic infiltration and severe jaundice, but not hydropic degeneration induced by aflatoxin B1. Cadmium increased the toxicity of warfarin with severe lameness, subcutaneous hematomas in the ventral surface of the neck, and death.

Aflatoxin B1↗
PubMed1982

Experimental Naegleria fowleri meningoencephalitis in sheep: light and electron microscopic studies.

A sheep infected intranasally with Naegleria fowleri of human origin died 7 days after inoculation. The olfactory lobes were distinctly soft and friable. Histologic findings indicated suppurative leptomeningitis and hemorrhagic necrosis in the olfactory lobes. Protozoa were disseminated in the necrotic areas, particularly in perivascular locations; vasculitis was also observed. Meningitis and perivascular cuffing with lymphocytes were evident in the cerebrum, cerebellum, pons, medulla, and cervical spinal cord. Electron microscopy disclosed trophozoites only in the olfactory lobes. The amebae contained a central nucleus with a distinct, electron-dense nucleolus. The cytoplasm contained myelinated figures, lipid-like vacuoles, open vesicles, electron-dense granules, mitochondria, numerous free ribosomes, scant rough endoplasmic reticulum, and occasionally a phagocytized erythrocyte. Trophozoites were grouped close to arterioles, except when phagocytized by a neutrophil or endothelial cell.

Amebiasis↗
PubMed1982

Ultrastructure of amastigotes of Leishmania donovani in the bone marrow of a dog.

Visceral leishmaniasis was diagnosed in a dog which had been in Spain for 4 years before being brought to Florida. A bone marrow aspirate from the dog was examined by electron microscopy. Phagocytized amastigotes by macrophages had an electron-dense plasma membrane and contained ribosomes, rough endoplasmic reticulum, a well-developed Golgi apparatus, an intracellular flagellum, lipid, a kinetoplast, a row of microtubules immediately beneath the cell membrane, and a nucleus with marginated chromatin. Mean diameter and microtubule number of the dog isolate were similar to those reported for Leishmania donovani amastigotes of human origin. Plasma cells were congregated in the vicinity of parasitized macrophages.

Animals↗
PubMed1982

Morphologic alteration of Anaplasma marginale in calves treated with a dithiosemicarbazone.

Blood and clotted blood samples from 3 calves with anaplasmosis were examined by light and electron microscopies before and after the calves were treated twice with alpha-ethoxyethylglyoxal dithiosemicarbazone (given IV). In the treated calves anaplasma bodies were swollen and irregularly shaped and had rough surfaces when viewed by light microscopy. Posttreatment electron microscopic examinations revealed swelling and vacuolation of initial bodies of anaplasma bodies, and ballooning of the vesicular membrane surrounding the anaplasma body. Other initial bodies were ameboid in shape this was or was not accompanied by rupture of the vesicular membrane of the anaplasma body. Necrotic, ameboid-shaped initial bodies also were seen. Some necrotic initial bodies were surrounded by complete vesicular membrane, and others were close to a broken, curled vesicular membrane.

Anaplasma↗
PubMed1981

Susceptibility of various poultry species to dietary aflatoxin.

1. The relative sensitivities of broiler chicks, White Leghorn chicks, quail chicks, goslings and turkey poults to increasing dietary contents of aflatoxin from 1 to 21 d of age were determined. Aflatoxin was included in the diets at three concentrations (0.7, 1.4 and 2.1 mg aflatoxin B1 equivalents/kg). 2. Data were analysed for species differences in food consumption, body weight, food utilisation, mortality and liver pathology. 3. There were no significant effects of aflatoxin in broiler and Leghorn chicks. Aflatoxin at 0.7 mg/kg decreased the body weight of turkey poults but tended to increase the growth rate of goslings. At 1.4 mg aflatoxin/kg food consumption, body weight and weight gain of goslings were adversely affected. 4. Liver damage occurred in goslings and quail chicks at all inclusions of aflatoxin and was extensive at 2.1 mg/kg. 5. Poults and goslings appeared to be the most sensitive, quail were intermediate and domestic chicks were most resistant.

Aflatoxins↗