Systemic candidiasis in a grey kangaroo.
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Biomedical subjects
Publications and source records attributed to J D Baird.
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Hyperbilirubinemia was present in 387 out of 1279 sick cattle admitted to the clinic of the Ontario Veterinary College. One hundred and ninety five of these had a total serum bilirubin of 17 mumol/L or greater. Clinical records, laboratory data and when available, pathology reports from these 195 animals were examined in an attempt to explain the reason for the high bilirubin levels. The hyperbilirubinemia in 187 of these was mainly due to an increase in unconjugated bilirubin. Jaundice, liver disease or anemia was not a feature and alkaline phosphatase was not elevated. The 195 animals with hyperbilirubinemia suffered from a variety of diseases that seemingly were unrelated to the increased bilirubin. The most frequently described signs were anorexia and rumen stasis. Liver disease was diagnosed in eight animals and in these clinical jaundice, and increased conjugated bilirubin and alkaline phosphatase was a feature. It was concluded that hyperbilirubinemia occurred in many diseases of cattle and in most instances was related to a failure of the liver to remove unconjugated bilirubin from the serum rather than to a failure of the liver to excrete conjugated bilirubin.
The relationships between (i) urinary free cortisol and urinary creatinine concentrations and (ii) the urinary cortisol/creatinine ratio (UCCR) and various glycaemic levels were studied in three groups--normal, insulin-stressed and insulin-treated diabetic subjects. In non-hypoglycaemic subjects, there was a significant positive linear correlationship between urinary free cortisol and urinary creatinine excretion, but in the presence of hypoglycaemia, this relationship was lost. The highest mean urinary cortisol/creatinine ratio (UCCR) was found in subjects after an insulin tolerance test (ITT). The mean post-ITT UCCR was significantly greater than the mean for the pre-ITT samples. There was a significant negative correlation between capillary blood glucose levels at 03.00 and the UCCR of the overnight urine samples of insulin-treated diabetic subjects. We conclude that there is a definite increase in the UCCR after hypoglycaemia in subjects with adequate adrenocortical response to hypoglycaemia and that determination of the UCCR could be helpful in the detection of nocturnal hypoglycaemia.
Rats implanted with progesterone gained weight more rapidly than controls and had a greater percentage of total body fat. The dietary intake of hormone-treated animals was restricted to control levels. The food was supplied in small quantities at regular intervals over a 24-h period with the aid of automatic feeding machines. The observed changes in body weight and composition are therefore not related to either an increased intake of energy or a change in the pattern of feeding after implantation.
Twelve pony foals (reared worm-free) were inoculated with Strongylus vulgaris. Approximately 8 weeks later, 4 of the foals were given fenbendazole (10% suspension) at a dosage rate of 10 mg/kg of body weight daily for 5 days and 4 foals were given the suspension at a dosage rate of 50 mg/kg daily for 3 days; the remaining foals were given a placebo. All treatments were administered by stomach tube. Fenbendazole was 99.6 and 97.9% effective in the 2 treatment groups, respectively, in eliminating later 4th-stage S vulgaris larvae located near the origin of major intestinal arteries. On microscopic examination of the ileocolic artery from fenbendazole-treated foals, a few larval remnants were found beneath the tunica intima in small organized mural thrombi overgrown with endothelium. It would appear that larvae are rapidly destroyed after administration of fenbendazole. A pony foal reared on pasture and with arteriographic evidence of arteritis of the cranial mesenteric and ileocolic arteries was treated with fenbendazole (10% suspension) by stomach tube at a dosage rate of 50 mg/kg of body weight daily for 3 days. By arteriographic examination made 4 weeks later, there was evidence of regression of the lesion, and at necropsy done a week later, there was no arteritis or larvae in the lumen of those arteries.
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Female rats implanted with progesterone gained weight more rapidly than control animals and had a greater percentage of total body fat. The proportion of fat in the carcase of control animals also increased as they gained weight. Comparison of progesterone-treated rats with a group of weight-matched controls demonstrated that the effects of progesterone treatment on fat deposition exceeded those which would be expected to accompany their accelerated growth. Excess fat was deposited at the expense of the protein component of fat-free solid.
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The oral administration of bromocriptine 5 mg 6-hourly to twelve patients with acromegaly for a mean period of 12 (range 3-27) months significantly reduced whole blood glucose, plasma insulin and plasma growth hormone (GH) concentrations during a 50 g oral glucose tolerance test (OGTT). After this period of treatment, bromocriptine was withdrawn for 48 h resulting in a significant rise in whole blood glucose, plasma insulin and plasma GH concentrations during a repeat OGTT. It is concluded that bromocriptine therapy improves glucose tolerance in acromegaly by suppressing GH secretion and consequently GH-mediated antagonism of insulin.
The susceptibility of a known thiabendazole-resistant population of small strongyles to anthelmintics of both benzimidazole and non-benzimidazole groups, was determined. In the first study, 42 horses infected with thiabendazole-resistant small strongyles were allocated to 6 groups. Treatment groups received one of the following anthelmintics: mebendazole, febantel, febantel plus trichlorphon, morantel tartrate, or a combination of thiabendazole, piperazine and trichlorphon. Morantel tartrate and the thiabendazole/piperazine/trichlorphon combination produced highly significant (p less than 0.001) reductions in faecal strongyle egg counts 20 days post-treatment. Mebendazole, febantel and febantel plus trichlorphon failed to reduce strongyle egg counts significantly. Larval culture and differentiation indicated that in all cases of anthelmintic failure, small strongyles of the sub-family Cyathostominae were involved. Eighteen horses from groups in which treatment had failed were re-allocated to 3 groups. Treatment with either morantel tartrate or haloxon was highly efficient in reducing faecal strongyle egg counts. In the final study, fifty-four horses, infected with benzimidazole-resistant small strongyles were allocated to 10 groups. On day zero, each treatment group received one of the following anthelmintics: thiabendazole, cambendazole, mebendazole, oxibendazole, piperazine, thiabendazole/piperazine, cambendazole/piperazine, mebendazole/piperazine or oxibendazole/piperazine. Oxibendazole, piperazine and the benzimidazole/piperazine combinations produced highly significant reductions in faecal strongyle egg counts 20 days post-treatment (p less than 0.001). When administered alone, benzimidazole anthelmintics failed to reduce strongyle egg counts significantly, with the exception of oxibendazole. Larval culture and differentiation indicated that in all cases of anthelmintic failure, the species involved were small strongyles of subfamily Cyathostominae. There was no significant increase in benzimidazole resistance level (based on in vitro assay) as a result of drug treatment, over one generation.
The plasma insulin response to glucose an arginine was increased in intact female rats implanted with progesterone. This change was not mediated by increased energy intake since the insulin response to glucose was similarly enhanced in progesterone-treated rats pair-fed with controls. In contrast, similar levels of pancreatic glucagon were observed in the plasma of both control and experimental rats during arginine stimulation. Thus the molar ratio of insulin to glucagon may be increased in the plasma of progesterone-treated rats following a mixed meal. This change may represent a physiological adaption to a demonstrable resistance to the peripheral actions of insulin in non-adipose soft tissue. The hyperglycaemic and lipolytic actions of exogenous glucagon were also impaired in progesterone-treated rats. It is suggested that an increase in the molar ratio of insulin to glucagon will favour hepatic lipogenesis and the peripheral deposition of fat.
Females rats implanted with progesterone gained weight more rapidly than control animals and had an increased proportion of total body fat. Restriction of food intake to control levels demonstrated that the weight changes was not dependent on increased energy intake. Serum concentrations of cholesterol, phospholipid and non-esterified fatty acid were raised in hormone-treated rats but triglyceride levels were normal. Endogenous production of triglyceride was also unchanged. Total postheparin lipoprotein lipase activity was increased in the plasma of progesterone-treated rats largely due to increased release of the extrahepatic protamine sulphate-labile fraction. The basal rate of lipogenesis was also increased in adipocytes isolated from hormone-treated rats as was the insulin-stimulated rate of oxidation of[1-14 C]glucose. Basal and adrenaline-stimulated rates of fat cell lipolysis were, however, unchanged by treatment with progesterone.
The effect of chlorpropamide on blood glucose, plasma insulin, C-peptide and glucagon levels was studied in 21 patients with insulin-independent diabetes. A metabolic profile of these parameters was obtained throughout a normal day in seven newly-diagnosed diabetic patients (group A), before, and 3 to 8 weeks after treatment with chlorpropamide was established, and in 14 patients on longterm therapy with chlorpropamide (seven taking less than 250 mg. chlorpropamide--group B; seven taking 250-375 mg.--group C), before, and two weeks after withdrawal of the drug. In group A, correction of hyperglycaemia was not accompanied by a significant rise in the mean plasma insulin and C-peptide levels but a fall was observed in the mean plasma pancreatic glucagon concentrations. In groups B and C, withdrawal of chlorpropamide produced no significant change in plasma insulin, C-peptide or glucagon levels, although the mean blood glucose increased. This study supports an extrapancreatic effect of chlorpropamide to lower blood glucose after prolonged administration. In the short-term, it is possible that chlorpropamide may influence the secretion of pancreatic glucagon.
Glycosylated haemoglobin (HbA1) was measured in seven insulin-dependent diabetic patients before, during, and after a seven-day period of monitored poor control. There was considerable individual variation in the pattern and degree of change in HbA1 concentration induced by poor control and the time when it occurred. Greater increases in HbA1 were seen during the period of metabolic derangement than in the subsequent two months. More information is required before HbA1 estimations are widely used clinically to monitor control in individual diabetics.
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The plasma concentration of C-peptide, insulin (IRI) and glucose was measured in 9 healthy subjects during insulin-induced hypoglycaemia followed by a meal. Identical observations were made in the same subjects after an equivalent period of fasting without hypolycaemia (control study). Endogenous secretion of insulin was suppressed following administration of exogenous insulin and this persisted long after the blood glucose concentration had returned to normal. After the meal the mean blood glucose rose to a peak of 8.4 +/- 0.3 mmol/l (mean +/- SEM) at 60 min and was still raised at 7.5 +/- 0.3 mmol/l at 120 min, compared with a peak value of only 5.1 +/- 0.2 mmol/l at 30 min after the meal in the control study. Following hypoglycaemia the mean plasma IRI rose from 8.3 +/- 1.3 mU/l to a delayed peak of 81.6 +/- 12.7 mU/l at 60 min and was 123.5 +/- 14 mU/l at 120 min post-prandially, compared with a peak of 72.4 +/- 0.5 mU/l at 30 min after the meal in the control study. Acute hypoglycaemia may thus induce in abnormal pattern of insulin secretion in response to a meal, with impaired carbohydrate tolerance in normal subjects.
Severe abnormalities of plasma electrolyte concentrations were observed in 4 children who had massive hyperlipidaemia secondary to poorly-controlled, insulin-dependent diabetes mellitus. These electrolyte values were fallacious and invoked problems of clinical management, particularly with regard to fluid replacement. Each case is described and the interpretation of plasma elecytolyte values in hyperlipidaemia is discussed.
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