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Biomedical subjects

C J Whitehead

Publications and source records attributed to C J Whitehead.

At least 19 recordsLinked to original sources
PubMed1995

Artificial transmission of Bolo disease in woolled sheep and attempted characterisation of the causative unclassified Corynebacterium sp.

Bacterial isolates (n = 38) previously cultured from sheep with Bolo disease were compared bacteriologically with known Corynebacterium spp. and Actinomyces spp. The isolates did not conform to any previously described species but closely resembled C. pseudodiptheriticum and C. urealyticum. More comprehensive tests are needed to classify this Corynebacterium sp. Bacterial cultures of this unclassified Corynebacterium sp. were used artificially to induce Bolo disease in Dohne Merino sheep (n = 20). Ten sheep were kept at Middelburg in the Cape Midlands (Northern Cape) under arid conditions and another 10 at Queenstown in the Eastern Cape in a more humid climate. Two suspensions containing 2.8 x 10(5) Corynebacterium sp. (inoculum A) and 2.8 x 10(9) Corynebacterium sp. (inoculum B) respectively were used to infect each sheep on 9 different sites on the skin. One sheep died during the course of the experiment. Corynebacterium sp. established itself on 81 out of 171 inoculation sites of the remaining sheep and caused typical lesions of Bolo disease, clinically and pathologically. Bolo disease lesions developed slowly over 175 days at Middelburg and 287 days at Queenstown. Weather conditions were unfavourable to the development of fleece-rot and mycotic dermatitis. No difference was seen in lesion development between rams and ewes or between sheep with 5 months' wool growth and those which were shorn before inoculation. More lesions developed with the higher concentration of inoculum B (49 sites positive) as compared to inoculum A (32 sites positive).

Actinomyces↗
PubMed1991

The effects of naloxone on the cardiovascular and respiratory effects of centrally administered corticotrophin releasing factor in conscious rabbits.

1. The effects of intracerebroventricular (i.c.v.) and intracisternal (i.c.) administration of corticotrophin releasing factor (CRF) (0.5 nmol kg-1) were examined in conscious rabbits. The effect of opioid receptor antagonism was examined to determine whether the responses to CRF were mediated by endogenous opioid peptides. 2. After i.c.v. CRF there was a rise in mean arterial pressure (MAP), heart rate (HR), plasma noradrenaline and adrenaline, and increased behavioural activity. Respiration rate increased, PaCO2 fell, but PaO2 was unchanged. 3. The pressor and behavioural effects of i.c.v. CRF were unaltered by high doses of intravenous naloxone (9 mumols kg-1 bolus followed by 9 mumols kg-1 min-1 infusion); these effects of CRF were also not prevented by double this dose of naloxone. Naloxone attenuated the CRF-induced tachycardia, blocked the increase in respiration rate and increased the fall in PaCO2. 4. After i.c. CRF (0.5 nmol kg-1) there were similar changes in MAP, HR, plasma catecholamines, respiration and behaviour. 5. These results indicate that in conscious rabbits the pressor effects of i.c.v. CRF are not mediated by endogenous opioid peptides. The finding that the effects of CRF were similar after i.c.v. and i.c. administration suggests that these responses may result from actions on brainstem rather than periventricular sites.

Animals↗
PubMed1991

The pressor response to central administration of beta-endorphin results from a centrally mediated increase in noradrenaline release and adrenaline secretion.

1. The effects of intracerebroventricular (i.c.v.) and intracisternal (i.c.) administration of beta-endorphin (0.01, 0.1 and 1.0 nmol kg-1) were examined in conscious rabbits. 2. After i.c.v. beta-endorphin, mean arterial pressure (MAP) increased, heart rate (HR) fell, plasma noradrenaline, adrenaline and glucose increased and there was a rise in PaCO2 and fall in PaO2; these effects were reversed by intravenous (i.v.) naloxone (300 nmol kg-1). 3. A combination of prazosin (2 mg kg-1) and yohimbine (1 mg kg-1), given i.v., prevented the rise in MAP induced by i.c.v. beta-endorphin. 4. After i.c. beta-endorphin, MAP, HR and plasma catecholamines were not significantly altered but there was a similar degree of respiratory depression. 5. Clonidine (1.0 micrograms kg-1, i.c.) reduced MAP and HR; these effects were not blocked by i.v. naloxone (6 mumol kg-1). 6. These results demonstrate that beta-endorphin acts centrally, probably mainly on periventricular mu-opioid receptors, to increase adrenaline secretion and sympathetic nerve activity leading to alpha-adrenoceptor-mediated vasoconstriction. The respiratory depression is probably mediated by brainstem mu-receptors. 7. A role for beta-endorphin in the central hypotensive action of alpha 2-adrenoceptor agonists was opposed by finding that opioid receptor antagonism with naloxone did not block the effects of clonidine.

Animals↗
PubMed1991

After the violation. Treating rape victims.

Rape is a devastating, violent crime that can occur to women and men of all ages, races and socioeconomic classes. For the prehospital provider, managing a sexual-assault victim requires special skills and knowledge to sensitively handle the patient's physical, mental and emotional symptoms and preserve evidence for trial.

Emergency Medical Services↗
PubMed1990

Functional and autoradiographic studies to locate the sites at which clonidine acts to cause hyperglycaemia and inhibition of opiate-induced sympathetic outflow.

The effect of intracisternal administration of clonidine (1 microgram/kg) on the response to intravenous injection of morphine (4 mg/kg) was examined in conscious rabbits. Morphine acts on central opiate receptors to increase sympathetic outflow and cause hypertension. Clonidine, given intracisternally, prevented the morphine-induced rise in mean arterial pressure, fall in heart rate and increase in catecholamines in plasma. Using in vitro autoradiography, alpha 2-adrenoceptors were localised in the nucleus of the tractus solitarius and the dorsal motor nucleus of the vagus and these may be two of the sites at which clonidine acts. Clonidine also causes hyperglycaemia after intravenous administration and the site of action was investigated by comparing the effects of intravenous and intracerebroventricular administration of clonidine (1, 2 and 2 micrograms/kg), given at intervals of 30 min. Similar increases in glucose occurred after intraventricular and intravenous administration of clonidine, indicating that it has both central and peripheral actions, which increase glucose by different mechanisms. Clonidine, given intraventricularly also reduced mean arterial pressure and heart rate but there were no effects after intravenous administration. These studies demonstrate that the inhibitory effect of clonidine on opiate-induced stimulation of sympatho-adrenal outflow is central, whereas the hyperglycaemic effect of clonidine depends on both central and peripheral mechanisms.

Animals↗
PubMed1990

Bolo disease: a specific, localised skin disease of woolled sheep.

Bolo disease is limited to Merino and Döhne merino sheep in the Stutterheim and Cathcart districts of the eastern Cape Province. It occurs under natural grazing conditions regardless of the season of the year and the condition of the natural grazing. Ewes and wethers are most frequently affected. Skin lesions are well-defined, and the corresponding fleece has dark-grey to almost black spots, patches or bands varying in number, size and distribution between individual sheep. The wool in the affected areas is visibly shorter, less dense and tender, and the tips of the staples are spiky. In freshly-shorn sheep, the affected areas appear chalky white. Chronic and superimposed acute lesions are present in the same specimen histologically. Skin lesions include superficial and follicular hyperkeratosis, acanthosis, and sebaceous gland hyperplasia and hypertrophy. These changes are accompanied by dilatation of some of the follicles in the midshaft area, and collapse of the subepidermal tissue with only a few remaining collagen fibres separating the follicles and the sebaceous glands from the thickened epidermis. Corynebacterium spp. is the most consistent bacterium isolated from the lesions. Lesions produced by suspensions of this organism simulated both clinical signs and histopathological findings of the natural condition.

Animals↗
PubMed1990

Bolo disease: a bacteriological survey.

A total of 718 sheep, 381 severely and 190 mildly affected with Bolo disease as well as 147 visibly unaffected animals emanating from 15 farms in the Stutterheim and Cathcart districts in the eastern Cape were subjected to bacteriological examination of skin surfaces and wool specimens. Altogether, 1,168 specimens were examined. These included skin swabs, skin scrapings and wool samples. Corynebacterium spp represented 94.4% of the primary isolates in cultures prepared from all specimens and 97.2% in those derived from skin swabs only, while a variety of other bacteria collectively constituted the remainder of primary isolates. In all, Corynebacterium spp was isolated from specimens of 94.2% of sheep severely affected with Bolo disease and from 83.7% of those mildly affected, whereas it could only be isolated from 1.36% clinically unaffected sheep. In a comparative study, swabs taken directly from the skin surface, proved to be the method of choice for the collection of specimens for bacteriological examination of Bolo disease. Using this method, Corynebacterium spp. was isolated from 98.7% of severely, and 85.3% of mildly affected sheep as well as 4% of sheep apparently unaffected by Bolo disease. The isolation of Corynebacterium spp. from skin scrapings collected from the 3 categories of affection (73.3%, 57.3% and 4% respectively) and from wool samples (52%, 41.3% and 1.3% respectively) proved these 2 methods of sampling to be less reliable. A close association has been established between the incidence of Corynebacterium spp. and the occurrence of clinical Bolo disease.

Animals↗
PubMed1989

Evidence that intravenous morphine stimulates central opiate receptors to increase sympatho-adrenal outflow and cause hypertension in conscious rabbits.

1. In conscious rabbits, intravenous morphine caused hypertension, bradycardia, hyperglycaemia and increased plasma adrenaline and noradrenaline. These effects were prevented by ganglionic blockade with pentolinium. 2. The cardiovascular responses to morphine were not altered by pretreatment with a vasopressin V1-receptor antagonist. 3. After bilateral adrenalectomy morphine caused a similar rise in noradrenaline but no increase in adrenaline. The rise in blood pressure was attenuated and the hyperglycaemia was abolished. 4. Adrenaline infused intravenously to mimic the levels that occurred after morphine caused a similar degree of hyperglycaemia but only a small increase in blood pressure. 5. Pretreatment with intracerebroventricular naloxone prevented the morphine-induced hypertension, hyperglycaemia, increase in plasma catecholamines, respiratory depression and sedation. 6. These results demonstrate that, in conscious rabbits, intravenous morphine causes hypertension by increasing sympathetic vasoconstrictor nerve activity and elevating plasma adrenaline levels; the latter alone produces the hyperglycaemia. Vasopressin release is not involved in the hypertensive response to morphine. The effects of morphine appear to result from stimulation of central opiate receptors leading to enhanced sympathoadrenal outflow.

Adrenalectomy↗
PubMed1989

Investigation of the central sites at which morphine acts to cause hypertension in conscious rabbits.

1. In conscious rabbits intracerebroventricular (i.c.v.) morphine (10 and 50 micrograms kg-1) caused a dose-related increase in plasma noradrenaline and adrenaline, respiratory depression and sedation. The increase in sympatho-adrenal outflow resulted in hypertension accompanied by bradycardia and the increase in adrenaline secretion caused hyperglycaemia. Morphine (1 microgram kg-1 i.c.v.) and i.c.v. saline had no effect. 2. The same doses of morphine given intracisternally (i.c.) caused bradycardia and a similar degree of respiratory depression to i.c.v. morphine, but no significant increase in blood pressure and only a small, gradual rise in plasma adrenaline. 3. Intravenous naloxone (1 mg kg-1) did not block the hypertension, hyperglycaemia or increase in plasma catecholamines that followed i.c.v. morphine, but prevented the respiratory depression and sedation. 4. Ganglionic blockade with pentolinium prevented the rise in plasma catecholamines, blood pressure and plasma glucose induced by i.c.v. morphine. 5. These findings demonstrate that the increased sympathoadrenal outflow following i.c.v. morphine results from an action on periventricular structures. The resultant increase in plasma catecholamines, which is largely naloxone resistant, accounts for the hypertension and hyperglycaemia. The bradycardia is probably partly baroflex mediated and partly due to an increase in vagal tone as a result of stimulation of brainstem opioid receptors. The respiratory depression is probably due to an action of morphine on brainstem opioid receptors.

Animals↗
PubMed1989

Differential cardiovascular and respiratory responses to central administration of selective opioid agonists in conscious rabbits: correlation with receptor distribution.

1. The effects of intracerebroventricular (i.c.v.) and intracisternal (i.c.) administration of a range of doses (0.01, 0.1 and 1.0 nmol kg-1) of specific mu- delta- and kappa-opioid agonists on cardiovascular and respiratory function and on plasma catecholamines have been studied in conscious rabbits. The distribution of mu- delta- and kappa-opioid receptors was localized in rabbit brain by in vitro autoradiography. 2. The mu-agonist [D-Ala2, MePhe4-Gly5-ol]enkephalin (DAGOL) given i.c.v. caused a large rise in plasma noradrenaline and adrenaline, hypertension accompanied by an initial bradycardia followed by tachycardia, respiratory depression and sedation. After i.c. administration there were similar changes in heart rate (HR) and respiration, but no significant changes in mean arterial pressure (MAP) or plasma catecholamines. 3. The delta-agonist [D-Pen2.5]enkephalin (DPDPE) increased MAP and HR after both i.c.v. and i.c. administration, caused a small increase in noradrenaline but had no effect on adrenaline and did not alter respiration rate or blood gases. After i.c.v. DPDPE the rabbits became more alert and active. 4. The kappa-agonist U69593 given i.c.v. or i.c. had no effect on MAP or HR. After i.c.v. U69593, PaCO2 fell, but there were no other respiratory effects. The responses to dynorphin 1-13, an endogenous kappa-agonist, were similar to those of U69593. 5. The opioid antagonist naloxone (30 nmol kg-1) given intravenously (i.v.) blocked the effects of i.c.v. DAGOL (1 nmol kg-1). A 100 fold higher dose of i.v. naloxone (3 mumol kg-1) was required to abolish the effects of i.c.v. DPDPE (1 nmol kg-1). 6. Autoradiographic studies demonstrated a high density of mu- and delta-opioid receptors in hypothalamic sites. In the brainstem mu-receptors were demonstrated in the nucleus tractus solitarius (NTS) and delta-receptors in the dorsal motor nucleus of the vagus. kappa-Receptors were not detected in either the hypothalamus or brainstem. 7. These findings demonstrate that DAGOL increases sympatho-adrenal outflow, probably by stimulation of hypothalamic mu-receptors. The effects on HR are probably partly through a baroreflex and partly through an action of DAGOL on mu-receptors in the dorsal motor nucleus of the vagus. DPDPE probably acts on delta-receptors in the NTS to increase MAP and HR. Respiratory depression resulted from stimulation of mu-receptors in the brainstem with no evidence of delta- or kappa-receptors being involved.

Animals↗
PubMed1989

Assessing key stakeholders: who matters to hospitals and why?

A key stakeholder perspective, informed by illustrative quantitative and qualitative data, is developed for hospital administrators. These data provide answers to the questions, Who matters to hospitals? and Why do they matter? A tool kit for assessing stakeholders also is presented to help hospital executives identify their institutions' key stakeholders, determine the power of these stakeholders and their core values, and define who within their institutions should be responsible for the routine management of different stakeholders. These tools facilitate the management of each key stakeholder, ensuring that each strategic decision is examined in terms of the likely reaction of key stakeholders and is supplemented with plans for gaining stakeholder acceptance. Managers should recognize that the answers to Who matters? and Why? will vary by type of hospital and by the specific issue being addressed.

Community-Institutional Relations↗
PubMed1989

A strategic approach for negotiating with hospital stakeholders.

Executives should consciously formulate negotiation strategies which are linked to the broader strategic posture of the hospital. This approach provides a diagnostic and action-oriented framework for (1) determining and focusing on desired outcomes and (2) anticipating actions stakeholders are likely to take.

Cooperative Behavior↗
PubMed1988

Cadmium-induced changes in avian renal morphology.

The effects of i.m. administered cadmium on growth rate and nephromorphology were studied in young pullets. The growth rate of pullets treated with 0.6 mg Cd2+/kg at 48-h intervals was severely retarded, reaching only 50% of normal growth by 21 days. Such a decrease in growth rate was prevented when cadmium was given with either ferric or magnesium EDTA chelate. Electron micrographs of kidney tissue from cadmium intoxicated birds revealed massive intracellular disorganisation of proximal tubular cells, showing increased vacuolation and dilated endoplasmic reticulum. Mitochondria were few and swollen with reduced cristae. Some disorganisation was noted in the group treated with MgEDTA in conjunction with cadmium, with normal morphology observed in the group treated with FeEDTA plus cadmium. In general, glomerular morphology of intoxicated pullets appeared normal, except that a 25% increase in thickness of the glomerular basement membrane was evident. No such membrane thickening was observed in any of the chelate treated groups. These findings indicate that both chelates can provide certain levels of protection, in terms of growth rate and morphology, from cadmium intoxication. The possible mechanisms by which chelates offer protection have been discussed, but many questions remain unanswered.

Animals↗
PubMed1988

Too many on the seesaw: stakeholder diagnosis and management for hospitals.

If hospital managers are to cope with the environmental turbulence and uncertainty facing hospitals, they must effectively manager their stakeholders. The stakeholder approach helps integrate managerial concerns normally treated separately, such as strategic management, marketing, human resource management, organizational politics, and social responsibility. This approach enables hospital executives to develop strategies for handling conflicting demands for effectiveness and efficiency from various stakeholders. Four generic strategies hospital managers can use depending on the type of stakeholder are detailed, and an overarching strategy for hospital managers is discussed.

Health Facility Administrators↗
PubMed1981

Bacterial contamination of warm carcase surfaces: the relation of total aerobic and coliform counts to the recovery of Escherichia coli I.

By an indirect contact method, the total numbers of aerobic and coliform bacteria and of Escherichia coli I per cm2 on the surfaces of warm carcases of 498 cattle, 426 sheep and 499 pigs were established. Total and E. coli I counts were classified in geometric progression, the classifications being used to monitor levels of contamination. The highest levels were found on pigs, E coli I was frequently isolated from pig surfaces and only sporadically from sheep and cattle. The recovery of E coli I was related to the overall extent of bacterial contamination. Levels of contamination and the prevalence of E. coli I are illustrated by bar-graph arrangements.

Abattoirs↗
PubMed1977

Meningeal worm-induced neurologic disease in black-tailed deer.

Neurologic disease attributable to Parelaphostrongylus tenuis was diagnosed in five black-tailed deer (Odocoileus hemionus columbianus) relocated from Oregon to Tennessee. Mortality occurred in the pre-release enclosure and in the release area. Infection with P. tenuis was considered the cause of an unsuccessful stocking attempt. In addition, neurologic disease was produced by experimental infection of a black-tailed x white-tailed deer hybrid. Clinical and pathologic findings were described for black-tailed and hybrid deer, and epizootiologic aspects of P. tenuis infections were discussed.

Animals↗