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Biomedical subjects

F W Edens

Publications and source records attributed to F W Edens.

At least 91 records · Page 5Linked to original sources
PubMed1976

Reduced symptoms of anaphylaxis in chickens by ACTH or heat.

Exogenous ACTH, when administered intramuscularly in four equal doses of 2 I.U./100 gm. of body weight at 24, 23, 22, and 21 hours prior to challenge with BSA, reduced the severity of anaphylaxis in BSA sensitized juvenile chickens. Additionally, a single heat exposure (45 degrees C.) of 30 minutes at 24 hours prior to challenge consistently reduced the severity of anaphylaxis. Single heating exposures at 24 hours prior to sensitization or at 48 hours prior to challenge did not influence the anaphylactic response. In one of two experiments single heat exposures at one hour prior to challenge reduced the severity of anaphylaxis. The levels of anti-BSA antibody which existed immediately prior to challenge were not affected by the heat treatments. These data demonstrate clearly that exogenous ACTH and a single, non-lethal heating episode, when applied 24 hours prior to the induction of anaphylaxis, reduced the severity of the symptoms associated with this particular hypersensitive reaction in the domestic chicken.

Adrenocorticotropic Hormone↗
PubMed1976

Modification of corticosterone and glucose responses by sympatholytic agents in young chickens during acute heat exposure.

In four experiments, immature Athens Randombred (ARB) chickens were maintained at a moderate temperature, (24 degrees C., 45% R.H.). In Exps. 1 and 2 reserpine was given intramuscularly (0.75 mg./kg.) 12 hours before the heating episode was begun; in Exp. 3, propranolol was given intravenously (4 mg./kg.) 2 hours before heating; and in Exp. 4, dihydroergotamine was given intramuscularly (4 mg./kg.) 6 hours before heating. Rserpine and propranolol elevated plasma corticosterone before the heating episode began, but dihydorergotamine did not. Reserpine also raised plasma glucose levels before heating, but propranolol and dihdroergotamine did not. During the heating episodes, plasma glucose and plasma corticosterone increased in non-drug-treated birds; the increases were then followed by significant declines. In birds treated with reserpine, propranolol, and dihydroergotamine, however, elevated plasma corticosterone was maintained throughout the period of heating. Propranolol and dihydroergotamine also stabilized plasma glucose at higher levels during heating, but reserpine permitted the late period decline similar to that of non-drug-treated birds. These results indicate an adrenal cortical insufficiency during heat stroke and death in young chickens.

Animals↗
PubMed1976

Body temperature and blood chemistry responses in broiler cockerels given a single intravenous injection of Na+ or Ca++ before an acute heating episode.

Eight-week-old broiler cockerels were injected intravenously with avian saline containing additional Na+ as NaCl or Ca++ as CaCl2. After the injections half of the chickens were heated at 45 degrees C. and the others were maintained at 24 degrees C. Cloacal body temperatures were determined and blood samples were collected before heat exposure and at 30 minute intervals until the chickens had been heated for 120 minutes. Na+ did not affect body temperature of chickens in the 24 degrees C. environment, but Na+-treated chickens in the 45 degrees C. environment had significantly elevated body temperatures compared to the heated controls. Ca++ caused a significant decrease in body temperature of the non-heated chickens, but it was without effect in heated chickens. Neither Na" nor Ca++ altered the responses of plasma glucose, cholesterol, and calcium during the heating episode. However, Ca++ caused a significant rise in plasma inorganic phosphate in non-heated chickens and prevented the rapid decline in the heated chickens. Na+ caused a significant fall in plasma inorganic phosphate in non-heated chickens, but it did not alter the plasma phosphate response to acute heat stress. The present experimental resultn chickens in a moderate temperature environment, and suggests that Ca++ initially exerts a peripheral rather than a central effect in decreasing the body temperature.

Animals↗
PubMed1975

Short-term effects of sodium pentobarbital on blood gases and chemistry in young chickens.

Sodium pentobarbital, in its commercially prepared propylene glycol-ethanol-saline vehicle, was given intravenously to 8-week-old male and female Athens Randombred chickens, and either the vehicle alone or 0.8% saline was given to similar groups. One minute after injection, blood samples were taken for blood pH, pCO2, HCO3 minus, corticosterone, total protein, or cholesterol levels. The pO2 was significantly lower in the pentobarbital-anaesthetized birds than in those given saline or the vehicle only. Plasma glucose of birds given the vehicle was elevated over that of those given pentobarbital or saline. Triglycerides were significantly higher in plasma of birds given pentobarbital or the vehicle. This increase appeared related to the presence of the glycol moiety in the vehicle.

Animals↗
PubMed1975

Enhanced immunosuppression in bursectomized chickens by passive transfer of antibody.

Three trials were conducted using commercial broiler cockerels to determine the immunological consequences of passive transfers of immune sera to bursectomized chickens. The data illustrate that passive transfers of immune sera to juvenile chickens which had been surgically bursectomized immediately after hatching caused a suppression of the primary hemagglutination response which was greater than that caused by bursectomy or passive transfer of immune sera alone. However, when these same birds were given a secondary challenge of antigen the resulting secondary hemagglutination response was normal. These data indicate that the passive transfer of immune sera to bursectomized chickens greatly limits their ability to mount primary humoral responses, while not affecting the ability to develop anamnestic immunity.

Animals↗
PubMed1975

Estimation of protein content in the plasma of young chickens by a refractometric method.

This study was conducted to evaluate a refractometric method for determination of protein content of chicken plasma. Comparison of the results obtained with the refractometric and the Lowry methods indicated that refractometry, when used with due caution in a typical laboratory situation, provided a simple, fast, inexpensive and valid method for determining the protein content of plasma from young chickens.

Animals↗
PubMed1975

Toxicity of dietary lead in Japanese quail.

The toxicity of dietary lead in Japanese quail was investigated. The data indicated that dietary lead, in the form of lead acetate, was toxic to young quail at the level of 500 p.p.m. and this toxicity was evidenced by an inhibition of normal growth and by anemia. The anemic state in the lead toxic quail was more readily detected by reduced blood hemoglobin concentrations than by packed cell volumes. In addition, the data suggested that lead interfered with normal sexual development in the males. Lead at levels as high as 1000 p.p.m. did not prevent normal primary antibody responses to sheep erythrocytes.

Animal Feed↗
PubMed1975

Effect on reserpine on humoral immune responsiveness in young chickens.

The role of reserpine in modifying a primary humoral immune response was evaluated in three experiments with young chickens. It was found that chickens injected with reserpine prior to an intravenous antigenic challenge with sheep red blood cells exhibited an enhanced primary humoral immune response. The enhanced response occurred concomitant with an elevation in adrenal cortical activity as evidenced by the significant elevation of serum corticosterone in the reserpine-treated chickens. These data suggest that both the adrenal cortex and medulla may influence immune responsiveness in the chicken.

Animals↗
PubMedDate not supplied

Isolation of a reovirus from poult enteritis and mortality syndrome and its pathogenicity in turkey poults.

Poult enteritis and mortality syndrome (PEMS) is an acute, infectious intestinal disease of turkey poults, characterized by high mortality and 100% morbidity, that decimated the turkey industry in the mid-1990s. The etiology of PEMS is not completely understood. This report describes the testing of various filtrates of fecal material from control and PEMS-affected poults by oral inoculation into poults under experimental conditions, the subsequent isolation of a reovirus, ARV-CU98, from one of the PEMS fecal filtrates, and in vivo and in vitro studies conducted to determine the pathogenicity of ARV-CU98 in turkey poults. In order to identify a filtrate fraction of fecal material containing a putative etiologic agent, poults were challenged in two independent experiments with 220- and 100-nm filtrates of fecal material from PEMS-negative and PEMS-positive poults. The 100-nm filtrate was chosen for further evaluation because poults inoculated with this filtrate exhibited mortality and significantly lower (P < or = 0.05) body weight and relative bursa weight, three clinical signs associated with PEMS. These results were confirmed in a third experiment with 100-nm fecal filtrates from a separate batch of PEMS fecal material. In Experiment 3, body weight and relative bursa and thymus weights were significantly lower (P < or = 0.05) in poults inoculated with 100-nm filtrate of PEMS fecal material as compared with poults inoculated with 100-nm filtrate of control fecal material. Subsequently, a virus was isolated from the 100-nm PEMS fecal filtrate and propagated in liver cells. This virus was identified as a reovirus on the basis of cross-reaction with antisera against avian reovirus (FDO strain) as well as by electrophoretic analysis and was designated ARV-CU98. When inoculated orally into poults reared under controlled environmental conditions in isolators, ARV-CU98 was associated with a higher incidence of thymic hemorrhaging and gaseous intestines. In addition, relative bursa and liver weights were significantly lower (P < or = 0.05) in virus-inoculated poults as compared with controls. Virus was successfully reisolated from virus-challenged poults but not from control birds. Furthermore, viral antigen was detected by immunofluorescence in liver sections from virus-challenged poults at 3 and 6 days postinfection and virus was isolated from liver at 6 days postinfection, suggesting that ARV-CU98 replicates in the liver. In addition to a decrease in liver weight, there was a functional degeneration as indicated by altered plasma alanine aminotransferase and aspartate aminotransferase activities in virus poults as compared with controls. Although this reovirus does not induce fulminating PEMS, our results demonstrated that ARV-CU98 does cause some of the clinical signs in PEMS, including intestinal alterations and significantly lower relative bursa and liver weights. ARV-CU98 may contribute directly to PEMS by affecting the intestine, bursa, and liver and may contribute indirectly by increasing susceptibility to opportunistic pathogens that facilitate development of clinical PEMS.

Animals↗
PubMedDate not supplied

Alterations in macrophage-produced cytokines and nitrite associated with poult enteritis and mortality syndrome.

Poult enteritis and mortality syndrome (PEMS) is an acute, transmissible, infectious intestinal disease associated with high mortality and morbidity in turkey poults. Earlier studies demonstrated immune dysfunction, involving both humoral and cell-mediated immunity, associated with PEMS. The current study examined cytokines and metabolites produced by macrophages from poults exposed to PEMS agent(s). Six trials were conducted with six separate hatches of poults. Poults in the PEMS group were exposed to PEMS agent(s) via contact exposure at 7 days of age whereas uninfected poults served as control poults. Abdominal macrophages were harvested from control (uninfected) and PEMS poults at various times postexposure and cultured for 18-24 hr in the presence of Escherichia coli lipopolysaccharide. Interleukin-1 (IL-1), interleukin-6 (IL-6), and tumor necrosis factor-alpha (TNF-alpha) bioactivities and nitrite levels in macrophage culture supernatants were quantified. Macrophage supernatants from PEMS poults had greater IL-1-mediated stimulation index compared with the macrophage supernatants from uninfected control poults in both trials. However, this increase was significant only in trial 1. IL-6 activity tested in three separate trials was significantly higher in PEMS macrophage supernatants over the controls. On the contrary, TNF-alpha production by macrophages was decreased in PEMS macrophage culture supernatants. Nitrite levels in PEMS macrophage culture supernatants were significantly higher in two out of three trials. These findings suggest that the enhanced production of proinflammatory cytokine/metabolites by activated macrophages in PEMS poults may be responsible, at least in part, for the physiological intestinal inflammation, gut motility, and anorexia that characterize this disease.

Animals↗
PubMedDate not supplied

Induction of functional defects in macrophages by a poult enteritis and mortality syndrome-associated turkey astrovirus.

The interaction of a poult enteritis and mortality syndrome (PEMS)-turkey astrovirus-Ohio State University (TAst-OSU) with the mononuclear phagocytic system cells, namely macrophages, was examined after in vitro and in vivo exposure. In vitro exposures were performed by incubating adherent turkey macrophages with various volumes of 10(6) 50% embryo infective dose (EID50)/ml TAst-OSU stock, whereas for in vivo challenge, poults were given a 200 microl inoculum of 10(6) EID50/ml TAst-OSU stock at 7 days of age. Results show that TAst-OSU in vitro exposure reduced macrophage viability relative to controls (P < 0.05) and decreased phagocytosis (P < 0.05) and intracytoplasmic killing of Escherichia coli (P < 0.05) after a 42-48-hr exposure. Poults challenged with TAst-OSU in vivo recruited almost 50% fewer Sephadex-elicited inflammatory cells in the abdominal cavity (P < 0.05) as compared with the sham controls. Similar to in vitro exposure, macrophages isolated from in vivo TAst-OSU-challenged poults exhibited reduced percentage of phagocytic macrophages (P < 0.05) as well as fewer intracytoplasmic E. coli per phagocytic macrophage (P < 0.05). TAst-OSU-challenged poults had a greater number of viable E. coli in their spleens (P < 0.05) after an intravenous E. coli challenge as compared with the non-TAst-OSU-challenged control poults. Macrophage-mediated cytokines and metabolites were also examined during this study. Both in vitro and in vivo TAst-OSU challenge resulted in reduced interleukin (IL)-1 and IL-6 activity. On the contrary, nitrite levels in macrophage culture supernatant fraction of TAst-OSU-challenged macrophages were significantly higher (P < or = 0.05). The findings of these studies indicated that TAst-OSU challenge induced defects in macrophage effector functions, implying that PEMS-turkey astrovirus can potentially impair the immune response of turkeys, thereby leading to enhanced susceptibility of turkeys to secondary, perhaps even fatal, bacterial infections.

Animals↗
PubMedDate not supplied

Effect of Bordetella avium infection on electrocardiograms in turkey poults.

Electrocardiograms (ECGs) were recorded from turkey poults infected with the W isolate of Bordetella avium. Strip chart data (amplitudes and intervals) were measured at 7, 14, 21, and 28 days postinoculation and compared with data from uninoculated controls. B. avium infection altered P-, RS-, and T-wave amplitudes, as well as P-R and S-T intervals throughout the 4-week experimental period. Heart rates were similar over the 4-week period in control poults, while rates in the infected birds were variable. Alterations in ECGs associated with B. avium infection appeared to be the result of disturbances in the cardiovascular system and may be associated with the pathogenicity of the organism in turkey coryza.

Animals↗