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Biomedical subjects

F W Edens

Publications and source records attributed to F W Edens.

At least 37 records · Page 2Linked to original sources
PubMed1997

Immune system dysfunction during exposure to poult enteritis and mortality syndrome agents.

Poult Enteritis and Mortality Syndrome (PEMS) is a condition of yet undefined etiology. Affected flocks may exhibit 100% morbidity with mortality up to 50% or more between 2 to 4 wk of age. The current study reports the immune status of poults experimentally infected with PEMS agent(s) in various trials. When compared with the unchallenged controls, PEMS-infected poults had significant atrophy of the bursa (up to 2-fold), thymus (up to 11-fold), and spleen (up to 2-fold) (P < or = 0.05). When challenged with SRBC, PEMS-infected poults had 1 to 2 log2 lower anti-SRBC antibody titers than the controls (P < or = 0.05). Responsiveness to a mitogenic lectin, phytohemagglutinin-P, was reduced significantly in PEMS poults (P < or = 0.05). These data show that the immune system of the poults is compromised significantly during PEMS infection in terms of lymphoid organ integrity and humoral and cell-mediated immunity. These findings imply, therefore, that immune dysfunction may contribute to the mortality observed during PEMS outbreaks.

Aging↗
PubMed1997

Atypical Escherichia coli strains and their association with poult enteritis and mortality syndrome.

To date, no definitive etiology has been described for Poult Enteritis and Mortality Syndrome (PEMS). However, two atypical Escherichia coli colony types are isolated consistently from moribund and dead poults afflicted with PEMS. To test the infectivity of these E. coli strains, poults were placed into floor pens in three isolation treatment rooms: 1) CONTROL: no bacterial challenge, 2) E. coli colony Types 1 or 2 posthatch oral challenge: 10(8) cfu/per poult at 1 d, and 3) E. coli colony Types 1 or 2 posthatch oral challenge: 10(8) cfu/per poult at 6 d. Daily intramuscular injections of cyclophosphamide (100 micrograms per poult) from 1 to 5 d posthatch were given to half of the poults in each treatment. Atypical E. coli challenge caused BW depression, and cyclophosphamide treatment exacerbated the response. All E. coli-challenged poults developed diarrhea similar to PEMS. Mortality was increased by both atypical E. coli colony types, but at 21 d E. coli colony Type 2 caused greater mortality than colony Type 1. With cyclophosphamide treatment, mortality was exacerbated with both colony types, but colony Type 2 at 1 d caused the greatest mortality. Ultrastructural damage to ileum epithelium cell microvilli and subcellular organelles indicated that part of the BW depression could be attributed to malabsorption of nutrients. It was concluded that the atypical E. coli colony Types 1 and 2 play a significant role in the PEMS disease.

Animals↗
PubMed1996

Glutathione S-transferases in the Japanese quail: tissue distribution and purification of the liver isozymes.

Cytosolic glutathione S-transferase (GST) activities toward 1-chloro-2,4-dinitro-benzene (CDNB), 1,2-dichloro-4-nitrobenzene (DCNB), ethacrynic acid (EA), 1,2-epoxy-3-(p-nitrophenoxyl)propane (EPNP), trans-4-phenyl-3-buten-2-one(t-PBO), delta 5-androstene-3,17-dione (ASD) and trans-stilbene oxide (t-SO); cytosolic glutathione peroxidase activity toward cumene hydroperoxide (CuOOH); and microsomal GST activity toward CDNB were examined in liver, kidney, brain, and lung of adult male and female Japanese quail. In all cases, the renal specific activity per milligram protein was higher than the hepatic activity and was the highest among the four tissues examined. No consistent sex differences in GST activity were observed. The GSTs were purified from quail liver cytosol by S-hexylglutathione and glutathione affinity chromatography. Total GSTs eluted from the S-hexylglutathione affinity column were further separated by chromatofocusing, and the microheterogeneity of the GST isozymes was shown by high-resolution native isoelectrofocusing (IEF) in polyacrylamide slab gels and by SDS-PAGE. Five subunits were identified: QL1 (30.5 kDa), QL2 (27.2 kDa), QL3a (26.8 kDa), QL3b (26.5 kDa), and QL4 (25.5 kDa). Western blot analysis revealed that QL1 and QL2 reacted with antibodies raised against the rat Mu class GSTs (Yb1 and Yb2), and QL3a and QL3b reacted with those raised against the Alpha class (rat Ya and mouse a). Substrate specific activity of each isoform was determined with CDNB, DCNB, CuOOH, EA, t-PBO, ASD, and t-SO. QL3a and QL3b have high reactivity toward CuOOH, while QL1 and QL2 showed high activity toward t-SO. The N-terminal amino acid sequence of QL2 was identical to that of the chicken Mu class GST subunit CL2. However, no sequence was obtained with QL1 due to possible N-terminal blockage.

Amino Acid Sequence↗
PubMed1995

Potassium chloride improves the thermotolerance of chickens exposed to acute heat stress.

Experiments were designed to test the hypothesis that chicks that drank an electrolyte solution containing K prior to and during an acute exposure to heat would have greater thermotolerance than chicks that consumed only water. In three experiments, 5- or 7-wk-old male chickens drank distilled water (control), or .3, .6, or .9% KCl solutions (Experiments 1 and 2), and .6 or .9% KCl or .8% KHCO3 solutions (Experiment 3) for 48 h before acute heat stress (HS) and during HS. Body temperature (Tb), blood pH, partial pressure of blood carbon dioxide (pCO2), ionized Ca (Ca2+), plasma Na, K, Cl, total Ca, inorganic P (Pi), and osmolality (Osm), and water consumption were determined. Water intake increased with the concentration of KCl. Before HS, .6% KCl increased plasma K and Ca2+, whereas .9% KCl resulted in a marked increase in K, Ca2+, Na, Cl, and Osm and a decrease in pH. During HS, .6% KCl-birds had lower hyperthermic Tb and pH values and higher Ca2+ and K concentrations than controls. Plasma Na and Osm of .6% KCl birds decreased whereas those of the control birds remained unchanged. Providing K as KHCO3 aggravated respiratory alkalosis and failed to influence either Tb or plasma electrolytes, suggesting that the beneficial effect of .6% KCl may in part be attributed to the accompanying Cl. Hyperthermic Tb and Ca2+ values were highly correlated. The results showed that .6% KCl solution reduced HS-related responses and indicated a relationship among supplemental KCl, blood Ca2+, and Tb.

Acid-Base Equilibrium↗
PubMed1994

Water-holding properties of thermally preconditioned chicken breast and leg meat.

A study was conducted to examine the effects of thermal preconditioning on the water-holding properties of chicken breast and leg meat. An initial experiment was performed by heat shocking (40 to 41 C for 1 h) and euthanatizing broilers at 3 to 6 wk of age. As seen commercially, heat caused higher drip loss, and the majority of this loss for breast (75 to 80%) and leg (90 to 100%) meat occurred within 3 d post-mortem. A second study with 6-wk-old broilers tested the following treatments: control (25 C), heat shock (40 to 41 C for 1 h), preconditioned control (3 consecutive d of exposure to 35 C for 3 h followed by a 21-h recovery between each exposure), and preconditioned (same as preconditioned control with an added heat shock on the final day). Thermal preconditioning did not circumvent the water-holding problems associated with heat shock. Meat from chickens exposed to heat lost significant amounts of drip during the crucial processing period--the first 6 h after death. In general, leg meat had lower drip loss and higher held water than breast, but cooked leg meat had lower held water. Treatment and meat type were significant (P < .05) in determining drip and cook loss. Preconditioned and heat shock breast meat appeared pale, soft, and exudative, similar to a condition found in pork. Thermal preconditioning does not prevent the loss in water-holding properties associated with heat.

Acclimatization↗
PubMed1994

Plasma growth hormone and prolactin response to FK 33-824, a synthetic opioid agonist, in broiler chickens.

A synthetic opioid agonist, FK 33-824 ([D-Ala2,N-Me-Phe4,Met-(O)5-ol]- enkephalin), was administered intramuscularly at levels of 0, 1, 25, or 625 micrograms/kg of body weight to 4-wk-old Arbor Acres x Arbor Acres broiler cockerels. All levels of FK 33-824 caused the birds to be sedated, with the highest dose causing deep sedation over the 240-min test period. A significant time by treatment interaction was seen for plasma growth hormone (GH). At 30 min after treatment, a significant increase in GH occurred, but this transitory increase returned to control levels at 60 min. A secondary GH peak was observed in the 240-min samples from cockerels given the 625 micrograms/kg dose. Significant treatment and time effects and a time by treatment interaction were seen in the plasma prolactin (PRL) response to FK 33-824. Prolactin was increased at 30 and 60 min after treatment with 1 microgram/kg, whereas higher doses seemed to suppress PRL concentrations. Over the 240-min experimental period, PRL concentrations tended to increase in all treatments except in the treatment with the lowest FK 33-824 dose, but the largest transitory increase was observed at 240 min in the birds given the 625 micrograms/kg dose. These results suggest that FK 33-824 affected GH and PRL secretion in chickens in a manner different from other opioid agonists. This difference was probably due to the ability of FK 33-824 to bind to multiple opiate receptors, with the highest affinity for mu receptors and lesser affinity for delta receptors, whereas other opioids have high affinity for delta receptors.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1993

Heat-stress response of broiler cockerels to manipulation of the gonadal steroids, testosterone and estradiol.

1. Estradiol supplementation resulted in heat-stress mortality in both intact and caponized cockerels accompanied by depressed plasma corticosterone. 2. Phenotype-selection for large comb and high plasma testosterone increased heat tolerance which was attributed to an increased plasma corticosterone. 3. The results suggested that the presence of testosterone had a positive influence on the heat tolerance of broiler cockerels.

Animals↗
PubMed1993

Calcium deficiency and food deprivation improve the response of chickens to acute heat stress.

The tolerance of chickens to acute heat stress may be modified by diet. Broiler chickens fed calcium-adequate (0.90% Ca) or -deficient (0.45% or 0.15% Ca) diets were either fed or not fed for 24 h and exposed to increasing temperatures (from 24 to 41 degrees C). Diets were fed for 7 d before heat stress in Experiment 1 and for 14 d before heat stress in Experiment 2. Body temperature, blood ionized Ca, pH, pCO2, plasma inorganic phosphate and total Ca were determined. During heat stress, Ca+2 and inorganic phosphate were depressed in all treatments. Feeding the 0.45% Ca diet for 7 d reduced hyperthermic body temperature of fed chickens but had no effect on body temperature of unfed chickens relative to the groups fed 0.90% Ca. No further improvement in body temperature response to heat stress was obtained by lowering the dietary Ca level to 0.15% or extending the feeding period to 14 d. Food deprivation was more effective in counteracting the heat-induced rise in body temperature than a dietary Ca deficiency. Heat-induced changes in body temperature, Ca+2, inorganic phosphate and blood pH were highly correlated (P < 0.001). The change in Ca+2 followed a pattern similar to that of changes in body temperature, but changes in inorganic phosphate seemed to be more indicative of changes in pH. Control birds fed 0.90% Ca exhibited the highest changes in Ca+2 and body temperature values. Feeding Ca-deficient diets reduced changes in both Ca+2 and body temperature. Unfed birds, regardless of dietary Ca level, showed the lowest changes in Ca+2 and body temperature.(ABSTRACT TRUNCATED AT 250 WORDS)

Acid-Base Equilibrium↗
PubMed1992

Heat shock protein response in phosphorus-deficient heat-stressed broiler chickens.

1. During acute in vivo heat stress, a normal heat shock protein (HSP) response was not inducible in chickens deficient in inorganic phosphorus (P(i)-deficient). 2. Small quantities of HSP 70 and HSP 90 were induced, but little or no HSP 23 was induced in P(i)-deficient chickens compared to P(i)-adequate chickens. 3. Increased susceptibility of P(i)-deficient chickens to acute heat stress was attributed to their inability to produce an adequate HSP response.

Animals↗
PubMed1991

Catecholamine- and endotoxin-influenced cutaneous basophil hypersensitivity in chickens.

1. Catecholamines suppress cutaneous basophil hypersensitivity (CBH) to intradermal phytohemagglutinin (PHA-P) challenge in chickens. 2. E. coli 0127:B8 endotoxin, reserpine, and propranolol prevented a norepinephrine-induced suppression of CBH. 3. PHA-P induced CBH appeared to be mediated through a beta-adrenergic receptor mechanism associated with plasma corticosterone in chickens.

Animals↗
PubMed1991

Tissue monoamine and plasma corticosterone concentrations following sympathetic alteration during acute endotoxicosis in chickens.

1. Splenic and heart ventricular NE levels and plasma corticosterone concentrations were increased following E. coli endotoxin administration in three-week-old chicks. 2. Chicks receiving either reserpine or propranolol injection before endotoxin exhibited increased NE in both tissues while only splenic 5-HT increased in birds receiving propranolol and endotoxin. 3. The effects of acute bacterial infection in chickens involves the peripheral nervous system neurotransmitters, NE and 5-HT, in the regulation of immune response.

Animals↗
PubMed1990

Tryptophan 2,3-dioxygenase activity in turkey poults infected with Bordetella avium.

1. Liver tryptophan 2,3-dioxygenase (TPO) activity was depressed significantly by the Bordetella avium infection localized in the trachea of the turkey poult. 2. Tryptophan, given orally, induced a significant increase in TPO activity in both control and infected poults. 3. Hydrocortisone induced TPO activity in the turkey in a dose dependent manner.

Animals↗
PubMed1990

Serum chemistries of Coturnix coturnix japonica given dietary manganese oxide (Mn3O4).

1. Plasma creatinine and inorganic phosphorus were increased in manganese oxide (Mn3O4)-treated adult male Coturnix quail, but BUN, BUN/creatinine ratio, uric acid, and total calcium were decreased. 2. Serum enzymes (alkaline phosphatase, glutamic oxaloacetic transaminase, glutamic pyruvic transaminase, and lactic dehydrogenase) were elevated in Mn3O4-treated adult male Coturnix quail, but creatine phosphokinase was not affected. 3. Dietary Mn3O4 at 5000 ppm did not produce overt signs of toxicosis.

Alanine Transaminase↗
PubMed1989

Effect of fasting and acute heat stress on body temperature, blood acid-base and electrolyte status in chickens.

1. The tolerance of chickens to acute heat stress, evaluated by the time required to reach the critical body temperature (Tr) of 44.5 degrees C, was markedly enhanced as the period of fasting was extended. 2. Fasting reduced the rates of heat-induced changes in blood acid-base and electrolyte status. 3. Changes in Tr were correlated with changes in blood pH, pCO2, [Cl-] and [Pi] but not with changes in [Na+] or [K+]. 4. Blood acid-base and electrolyte status were related to Tr rather than time of exposure to heat stress.

Acid-Base Equilibrium↗
PubMed1989

Blood plasma catecholamine concentration of poult embryos during the transition from diffusive to convective respiration.

1. Plasma catecholamines were determined in turkey embryos. 2. Decreased eggshell permeability depressed dopamine and epinephrine, but increased permeability also depressed epinephrine. 3. Norepinephrine (NE) was greatest before transition to convective respiration when hypoxia occurs. 4. NE was associated inversely with eggshell permeability. 5. Catecholamines appear to assist the embryo during hatching hypoxia.

Animals↗
PubMed1989

Lead influences on physiological and growth responses in Coturnix coturnix japonica selected for large body weights.

Coturnix coturnix japonica, selected for large adult weight (Fatty), were 40% heavier than random-bred controls (RB). Given dietary lead (50 or 500 mg/kg) from hatching, fatty (10%) showed a smaller decrease in body weight than did RB (22%) at 6 weeks. Egg production was lower in Fatty, and lead (500 mg/kg) caused a greater suppression in Fatty. Lead added to the diet of Fatty and RB control diets at 7 weeks into egg production caused a 15% decrease in RB production but only a transitory decrease in Fatty. Removal of lead from the diets at 7 weeks into production allowed RB to increase egg production 6-7 weeks later but no change was seen in Fatty. Plasma calcium was reduced in lead-exposed Fatty and RB, and removal of lead from the diets allowed only a small increase in calcium. After 15 weeks production, plasma calcium in lead-treated Fatty was approaching control levels. Femur weight was greater in Fatty, but lead caused an increase in both RB and Fatty femur weight. Removal of lead from the diet allowed only minimal recovery of femur weight. Male and female Fatty responses to dietary lead were parallel. These data indicate that Fatty was less sensitive to dietary lead than RB even though more lead per unit of metabolic mass was consumed.

Animal Feed↗
PubMed1988

Possible brainstem involvement in the modification of thermoregulatory processes by chlordecone in rats.

The involvement of the central nervous system in the hypothermia induced by chlordecone was studied by evaluating the effects of infusions of chlordecone injected into the lateral and third ventricles and the cisterna magna on colonic temperature (Tcol). Compared to rats given vehicle, infusions of 40, 320 or 800 micrograms of chlordecone into the lateral ventricle or 320 or 800 micrograms of chlordecone into the third ventricle, through chronic indwelling cannulae, did not change significantly Tcol. However, intracisternal infusions of 80, 160, 320 or 800 micrograms of chlordecone produced significant hypothermia (maximally 2.2 degrees C) which persisted for as long as 6 hr. Intracisternal infusions of chlordecone also produced a rapid increase in the temperature of the tail skin (Tsk) which persisted throughout the period of hypothermia. This suggests that the hypothermia produced by central administration of chlordecone is related to peripheral vasodilation. Since chlordecone has been reported to induce release of NE in the brainstem, and NE is known to modulate tonic vasomotor control in the medulla, the effects of NE infused intracisternally were studied. Intracisternal infusions of NE (16 micrograms) significantly decreased Tcol and increased Tsk, supporting the hypothesis that hypothermia induced by chlordecone is associated with vasodilatory effects, mediated by an adrenergic mechanism in the brainstem.

Animals↗