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PubMedDate not supplied

An outbreak of fowl cholera in ring-necked pheasants (Phasianus colchicus).

A total of 120 ring-necked pheasants from a 3000-bird flock in Zeeland, MI, died over a 3-day period. Clinical signs included sudden death, diarrhea, and limping. At necropsy, hepatomegaly with multifocal cream-colored foci randomly distributed throughout the parenchyma was observed in diseased birds. Additionally, the spleen was enlarged up to three times its normal size and had a marbled appearance. Microscopically, there was multifocal splenic and hepatic necrosis with intralesional rod-shaped bacteria. Pasteurlla multocida serotype 3/4 was isolated from liver and spleen. In this paper, we report an outbreak of acute fowl cholera in ring-necked pheasants.

Animals↗
PubMedDate not supplied

Outbreak of Fowl cholera in Baikal teals in Korea.

Fowl cholera (FC) caused by Pasteurella multocida was diagnosed in waterfowl, Baikal teals (Anas formosa), submitted to the National Veterinary Research and Quarantine in Korea. The total number of mortalities was 13,228 out of approximately 100,000 birds that wintered in Cheonsoo Bay, the most important habitat area of Baikal teals in the world. Clinical signs were detected in only a few birds because of sudden death. Grossly, the dead Baikal teals had lesions consistent with FC, including multifocal necrotic foci in the liver with enlargement, petechial or ecchymotic hemorrhages on the heart, and mucoid exudates in the duodenal mucosa. Microscopically, there were hepatocytic necrosis with bacterial colonization, hemorrhage and necrosis in the myocardium, and hemorrhagic enteritis. Pasteurella multocida was isolated from the liver and the heart of all birds examined, and the isolate (P-627) was the serotype 1 X 12 X 13 by the agar gel immunodiffusion test. In order to estimate the virulence of P-627, 5-wk-old commercial ducks were exposed intramuscularly or intratracheally to the bacterium. On the basis of mortality rate, the isolate, P-627, was found to be highly virulent. This is the first report of an outbreak of FC in Baikal teals in Korea.

Animals↗
PubMed1990

Feedback-inhibition of growth hormone (GH) secretion in fowl: GH-induced down-regulation of thyrotrophin-releasing hormone binding to pituitary membranes.

Administration of ovine GH to immature domestic fowl blunted their subsequent GH response to thyrotrophin-releasing hormone (TRH), a GH secretagogue in birds. The in-vivo administration of GH also reduced the ability of radiolabelled TRH to bind to plasma membranes of the pituitary caudal lobe, in which GH cells predominate. These inhibitory effects of GH were mediated by extrapituitary actions, since GH had no direct inhibitory effects on TRH-induced GH release or on pituitary TRH binding in vitro. GH inhibition of GH secretion and TRH binding would not appear to be mediated by hypothalamic somatostatin (SRIF) or peripheral somatomedin (IGF-I), since SRIF and IGF-I had no direct effects in vitro.

Animals↗
PubMed1990

Thyroidal inhibition of growth hormone secretion in fowl: tri-iodothyronine-induced down-regulation of thyrotrophin-releasing hormone-binding sites on pituitary membranes.

The number, but not affinity, of binding sites for [3H]3-methyl-histidine2-TRH ([3H]Me-TRH) on chicken adenohypophysial plasma membranes was increased in chickens made hypothyroid by goitrogen (methimazole) treatment (50 mg/kg per day for 7 days), which also increased circulating GH concentrations. Daily i.p. injection of thyroxine (T4; 100 micrograms/kg for 7 days) had no effect on [3H]Me-TRH binding to pituitary membranes, although it suppressed endogenous GH secretion. Binding of [3H]Me-TRH to pituitary caudal lobe membranes was, however, suppressed by tri-iodothyronine (T3) injected chronically (100 micrograms/kg per day, i.p., for 7 days) or acutely (100 micrograms/kg, 2 h before being killed). The suppression of [3H]Me-TRH binding and inhibition of GH secretion following T3 administration was dose related. Binding of [3H]Me-TRH to caudal lobe membranes was also suppressed following the incubation of pituitary glands with T3 in vitro, and the response was both dose and time related. These results suggest that T3 inhibits GH secretion in fowl by a down-regulation of pituitary TRH receptors. However, other mechanisms are involved in thyroidal inhibition of GH release in birds, since T4 had no effects on [3H]Me-TRH binding yet suppressed GH secretion in vivo.

Animals↗
PubMed1975

Aspects of the adrenal function in the domestic fowl.

Chromatographic purification of extracts of hen peripheral plasma on Florisil columns before measurement by spectrofluorometry showed a basal level for corticosterone of 1-3 mug/100 ml, which is much lower than concentrations previously reported using acid fluorescence. Neither handling, restraint nor repeated bleeding affected the concentration of this hormone or of glucose. Adrenal function tests with two preparations of synthetic corticotrophin showed that they caused a rapid rise in blood corticosterone and eventually of glucose. Results of studies using insulin or tolbutamide i.v. suggest that there is a threshold concentration of plasma glucose (about 70 mg/100 ml) below which hypoglycaemia stimulates the hypothalamic-pituitary-adrenal system in fowls. Prolonged treatment of laying hens with protamine zinc insulin led to aphagia and cessation of egg-laying; increased concentrations of corticosterone were observed 2 days after the administration of insulin ceased, coinciding with the return to normal plasma levels of glucose. 'Chemical adrenalectomy' with metyrapone showed that the restoration of plasma glucose to a normal concentration after insulin treatment is dependent upon fully functional adrenal cortical tissue. It appears likely that the adrenal medulla is a target for corticosterone which probably regulates the tissue levels of phenylethanolamine-N-methyltransferase, one of the enzymes necessary for the biosynthesis of adrenaline.

Adrenal Cortex Function Tests↗
PubMed1978

Influence of fasting, glucose and insulin on the levels of growth hormone and prolactin in the plasma of the domestic fowl (Gallus domesticus).

The concentrations of both GH and prolactin in the circulation of the domestic fowl have been determined after various treatments known to affect carbohydrate metabolism. Fasting decreased the level of glucose, stimulated the secretion of GH and inhibited the secretion of prolactin. Administration of insulin significantly depressed the level of GH in the plasma of normal or fasted birds and also in chickens which had received simultaneous injections of glucose or 2-deoxy-D-glucose. No consistent effect of insulin on the secretion of prolactin was observed. Hyperglycaemia subsequent to administration of glucose had no effect on the levels of either GH or prolactin. Glucagon-induced hyperglycaemia suppressed the level of GH in the plasma and stimulated that of prolactin.

Animals↗
PubMed1979

Acute effects of aldosterone on water and electrolyte transport in the colon and coprodeum of the domestic fowl (Gallus domesticus) in vivo.

White Leghorn laying hens were maintained on commercial poultry food (medium-Na+ diet) and fresh water. High-Na+ diet birds received, in addition, 10 ml 9% (w/v) NaCl/kg by stomach load for 2 days before perfusion experiments. The lumen of the coprodeum and colon of anaesthetized birds was perfused with a hyperosmotic solution resembling ureteral urine. Transmural solute and water fluxes and potential difference (p.d.) values were measured for 2.5 h before and for 8 h after i.v. injection of aldosterone (120 microgram/kg). After administration of aldosterone, the lag, increasing and stabilized plateau phases were identified for Na+, K+ and Cl- fluxes (which together formed an electroneutral ion-exchange system); plateau flux values were significantly greater than preinjection values and were comparable to values for birds maintained on low-Na+ diets in parallel experiments. Ammonium, phosphate and water fluxes were unresponsive to aldosterone and p.d. values showed a transient increase in medium-Na+ diet birds only. In parallel experiments on birds on low sodium diets the ammonium flux and p.d. increased but the osmotic flow and phosphate transfer did not respond. Therefore acute injection of aldosterone reproduced some but not all of the responses to dietary Na+ restriction in fowls.

Aldosterone↗
PubMed1979

Chronic aldosterone therapy and the control of transepithelial transport of ions and water by the colon and coprodeum of the domestic fowl (Gallus domesticus) in vivo.

White Leghorn laying hens were maintained on commercial poultry food (medium-Na+ diet) and fresh water. Birds maintained on a high-Na+ diet received, in addition, 10 ml 9% (w/v) NaCl/kg by stomach load for 2 days before the perfusion experiments. Some birds on each dietary Na+ level also received aldosterone injections (60 micrograms/kg per day, i.m.) for 2 days before the perfusion experiments. The lumen of the coprodeum and colon of anaesthetized birds was perfused with solutions resembling ureteral urine, with systematically varied Na+, NH4+, Cl- and osmotic concentrations. Aldosterone enhanced net Na+ absorption (JNa) and associated net Cl- absorption and K+ secretion, and induced (in birds on medium- but not on high-Na+ diets) the appearance of a saturable JNa component dependent on the luminal concentration of Na+. Aldosterone enhanced net absorption of NH4+ and decreased the transmural potential difference in birds on a high-Na+ diet only; water and phosphate fluxes were not affected. Disparities between aldosterone- and Na+-depletion-induced effects suggested that one or more factors (in addition to aldosterone) are involved in the normal mediation of the responses of the lower intestine of the domestic fowl to varied Na+ intake.

Aldosterone↗
PubMed1981

Estimation of thyroidal radioiodide clearance in the domestic fowl (Gallus domesticus).

A method for estimating thyroidal clearance of radioiodide from the blood plasma of the domestic fowl is described. It differed from published methods in a number of ways. (1) It utilized total thyroid radioiodide concentration (IT) and did not require the use of goitrogens or the separation of free and protein-bound components. (2) Radioiodide was injected intravenously rather than by other routes. (3) Plasma radioiodide concentration (IB) was determined from several serial samples from each bird rather than once only. (4) The method allowed the clearance constant (kappa; microliter/min per mg) to be estimated for individual birds, rather than from groups, thereby enabling effective replication for comparative experiments. The constant was estimated from the model dIT/dt = kappaIB, measurements being made within 120 min after injection to ensure that exit of radioiodide from the thyroid was negligible. The improved method resulted in estimates of clearance constants which agreed well with published findings.

Animals↗
PubMed1981

Inhibition of growth hormone release by prostaglandins in immature domestic fowl (Gallus domesticus).

The effect of prostaglandin (PG) E1, PGE2 and PGF2 alpha on GH secretion has been assessed in immature domestic fowl. The intravenous or subcutaneous administration of PGE1 and PGE2 (at a dose of approximately 200 microgram/kg) to 2-, 6- and 8-week-old cockerels consistently lowered plasma GH concentrations. This inhibition in GH secretion was observed for at least 40 min after administration of PGE1 and PGE2. The same dose of PGF2 alpha suppressed plasma GH levels in 2- and 6- week-old birds but the magnitude and duration of this response was less than that induced by PGE1 and PGE2. At this dose, administration of PGE1 and PGE2 resulted in overt signs of distress (e.g. gaping, panting, eye closure and postural instability) within 5-10 min of injection and the birds appeared to be sedated thereafter. Prostaglandin F2 alpha and lower doses of PGE1 and PGE2 did not have any apparent effect on behavior. These results suggest that prostaglandins inhibit GH secretion in birds although this may reflect a non-specific stress response.

Alprostadil↗
PubMed1982

3 beta-hydroxy-delta 5-steroid dehydrogenase activity in the rapidly growing ovarian follicles of the domestic fowl (Gallus domesticus).

The total and specific activity of 3 beta-hydroxy-delta 5-steroid dehydrogenase, isocitrate dehydrogenase (NADP+) and glucose-6-phosphate dehydrogenase were measured in ovarian follicles from the domestic fowl. The enzymes were assayed in the five largest yolk-filled follicles which were sampled twice during the ovulatory cycle, at 1 h and 16 h before an expected ovulation. The total and specific activity of granulosa enzymes increased throughout the hierarchy and reached a maximum in the largest follicle. The relative increase in 3 beta-hydroxy-delta 5-steroid dehydrogenase activity was greater than that of the other two enzymes examined. The total thecal 3 beta-hydroxy-delta 5-steroid dehydrogenase activity reached a maximum in the third and fourth largest follicles. Thereafter its activity decreased up to the time of ovulation. The activity of 3 beta-hydroxy-delta 5-steroid dehydrogenase and glucose-6-phosphate dehydrogenase in follicles collected 1 h before and ovulation were significantly less than the activity in corresponding follicles collected 16 h before an ovulation.

3-Hydroxysteroid Dehydrogenases↗
PubMed1983

Thyroid hormones inhibit growth hormone secretion in domestic fowl (Gallus domesticus).

The influence of thyroxine (T4) and tri-iodothyronine (T3) on the secretion of GH in immature fowl was investigated. In birds pretreated with i.m. injections of T4 (100 micrograms/day for 10 days or 250 micrograms/kg for 7 days) or T3 (250 micrograms/kg for 7 days) the basal plasma GH level was markedly reduced. A similar reduction in the basal plasma GH level was also observed 60 min after a single injection or T3 (25 and 250 micrograms/kg) or T4 (250 micrograms/kg). In control birds the concentration of plasma GH was greatly increased (greater than 450 micrograms/l) within 10 min of an i.v. injection of thyrotrophin releasing hormone (TRH; 10 micrograms/kg). In birds pretreated with T3 or T4 the increase in GH concentration after TRH treatment was significantly less than that in the controls. In birds pretreated for 60 min with T3 or T4 the GH response to TRH was inversely dose-related and lowest in T3-treated birds. These results demonstrate that T3 and T4 inhibit GH secretion in birds, which is an effect not observed in mammalian species.

Animals↗
PubMed1984

Ovarian aromatase activity in the domestic fowl (Gallus domesticus).

Fowl ovarian aromatase activity was measured by an assay based on the stereospecific elimination of tritium from [1,2-3H]testosterone. The production of tritiated water was shown to provide a valid estimate of aromatase activity under the conditions used. The small yellow follicles and ovarian stroma contained 50% of the total ovarian aromatase activity. The activity in the thecal tissue from the rapidly growing follicles reached a maximum level in the fourth largest follicles (17% of the total ovarian activity) and thereafter declined to low levels in the largest follicle and first post-ovulatory follicle. No activity was detected in the granulosa tissue from the rapidly growing follicles. It is proposed that the basal levels of plasma oestrogen in hens are maintained by production in the small yellow follicles and/or ovarian stroma. The variation in plasma oestrogen during the ovulatory cycle probably arises from secretion by the rapidly growing follicles.

Animals↗
PubMed1984

Brain sites involved in the regulation of growth hormone secretion in the young male domestic fowl.

To study brain sites involved in the regulation of GH secretion in the domestic fowl, lesions were placed in and around the hypothalamus of 1-week-old cockerels. Circulating concentrations of GH were then measured at weekly intervals for 4 weeks after the placement of lesions. At the termination of the experiment, histological procedures were used to determine the exact site of the lesion in each bird. Although a fair degree of overlap existed between the lesion sites leading to stimulation and those causing an inhibition of GH secretion, a clear distinction could be made in the overall distribution of stimulatory and inhibitory sites of GH control. A high concentration of lesion sites resulting in GH decline (presumed GH-releasing factor-rich areas) appeared to reside in the general area of the ventromedial and the arcuate nucleus of the hypothalamus. Lesion sites causing a GH rise (presumed somatostatin-rich areas), on the other hand, seemed to have a more caudal distribution. In addition, some evidence of an anterior hypothalamic distribution of these presumed 'somatostatin' neurones was observed. These agree with the existing immunohistochemical data on the distribution of somatostatin and constitute experimental evidence for localization of presumed GH-releasing factor sites within the avian brain.

Animals↗
PubMed1985

Mechanisms of release of prolactin from fowl anterior pituitary glands incubated in vitro: effects of calcium and cyclic adenosine monophosphate.

Fowl anterior pituitary glands were bisected and each half was pretreated in either Medium 199 or medium containing EGTA to deplete endogenous calcium (Ca2+) stores, after which they were incubated in Medium 199, or Ca2+-free medium, containing prolactin release-stimulating agents and verapamil, a Ca2+ channel blocker. High K+ concentrations, hypothalamic extract, synthetic thyrotrophin-releasing hormone (TRH) and dibutyryl cyclic AMP (dbcAMP) all stimulated release of prolactin from control (non EGTA-treated) hemianterior pituitary glands. The effects of TRH and dbcAMP were not additive, but the response to submaximal concentrations of TRH was augmented by theophylline, a phosphodiesterase inhibitor. Reduction of Ca2+ availability with EGTA or verapamil reduced basal release of prolactin, prevented the prolactin-stimulating effects of high K+ concentrations and TRH, and markedly attenuated responses to hypothalamic extract and dbcAMP, EGTA being more effective than verapamil. Increasing the Ca2+ concentration of the medium did not augment basal or stimulated release of prolactin. These results suggest that both Ca2+ and cyclic AMP may act as intracellular mediators in the release of prolactin. Both basal and stimulated release of prolactin depend upon the presence of Ca2+. Although influx from the medium may be the major source of Ca2+, endogenous stores of Ca2+, perhaps mobilized by dbcAMP, may be able to maintain some release of prolactin. The prolactin-stimulating effects of TRH may be mediated by cyclic AMP.

Animals↗
PubMed1985

Physiological control of growth hormone secretion by thyrotrophin-releasing hormone in the domestic fowl.

Immature cockerels (4- to 5-weeks old) were passively immunized, with antiserum raised in sheep, against thyrotrophin-releasing hormone (TRH). The administration of TRH antiserum (anti-TRH) at doses of 0.5, 1.0 or 2.0 ml/kg lowered, within 1 h, the basal concentration of plasma GH for at least 24 h. The administration of normal sheep serum had no significant effect on the GH concentration in control birds. Although the GH response to TRH (1.0 or 10.0 micrograms/kg) was not impaired in birds treated 1 h previously with anti-TRH, prior incubation (at 39 degrees C for 1 h) of TRH (20 micrograms/ml) with an equal volume of anti-TRH completely suppressed the stimulatory effect of TRH (10 micrograms/kg) on GH secretion in vivo. These results suggest that TRH is physiologically involved in the hypothalamic control of GH secretion in the domestic fowl.

Animals↗
PubMed1986

Serotoninergic inhibition of LH secretion in the domestic fowl.

Immature cockerels were injected with drugs known to affect serotoninergic activity. The receptor agonist quipazine as well as pargyline, an inhibitor of serotonin breakdown, both reduced plasma LH concentrations in a time-dependent fashion. The effect of pargyline was also dose-related. The serotonin precursor, tryptophan, reduced plasma LH levels. Tryptophan and pargyline were as effective in pubertal cockerels as in 3-week-old birds. Responses to quipazine were attenuated by the antagonist, methysergide, although another antagonist, cyproheptadine, also reduced plasma LH levels. Serotonin itself had no effect on plasma LH levels. Parachlorophenylalanine, which blocks serotonin synthesis, had no effect on plasma LH by itself, but attenuated the tryptophan-induced inhibition of LH. These data indicate that serotoninergic mechanisms inhibit secretion of LH in domestic fowl. This mechanism probably operates through the central nervous system.

Animals↗
PubMed1987

Serotoninergic regulation of corticosterone secretion in domestic fowl.

The effects of serotoninergic drugs on adrenocortical function in domestic fowl were examined. Administration of the serotonin receptor agonist 2-(1-piperazinyl)quinoline maleate (quipazine), an inhibitor of serotonin metabolism, N-methyl-N-2-propynylbenzylamine HCl (pargyline), as well as serotonin itself, all increased plasma concentrations of corticosterone. The maximum responses to serotonin and quipazine occurred 1 h after treatment. The quipazine-stimulated response was partly prevented by the serotonin antagonist cyproheptadine. Cockerels pretreated with dexamethasone, a synthetic steroid known to inhibit pituitary ACTH release, showed attenuated responses to subsequent quipazine, pargyline or serotonin injection. Serotonin, quipazine and cyproheptadine did not affect corticosterone release directly from the adrenal gland incubated in vitro, nor did they affect adrenal responsiveness to ACTH stimulation. The neurotoxin 5,6-dihydroxytryptamine injected into day-old chicks decreased plasma concentrations of corticosterone for up to 7 days after treatment, with corresponding decreases in the hypothalamic concentration of serotonin, but not dopamine or noradrenaline concentrations. These results show that adrenal corticosterone secretion is regulated by a central serotoninergic system, probably acting on the hypothalamo-pituitary-adrenal axis.

5,6-Dihydroxytryptamine↗