F. W. Edens

Influence of selenium sources on age-related and mild heat stress-related changes of blood and liver glutathione redox cycle in broiler chickens (Gallus domesticus)

Selenium is an essential trace element that up-regulates a major component of the antioxidant defense mechanism by controlling the bodys glutathione (GSH) pool and its major Se-containing antioxidant enzyme, glutathione peroxidase (GPX). Evidence has emerged suggesting that organic selenium, natural seleno-amino acids found in plants, grains and selenized yeast, maintains the antioxidant defense system more efficiently than inorganic selenium. Inorganic selenium is a pro-oxidant, whereas organic selenium possesses antioxidant properties itself. As a pro-oxidant, inorganic selenium is not suitable for animals or humans. Therefore, we examined the GSH-GPX system in broiler chickens and determined that organic selenium was indeed more beneficial than inorganic selenium. Chickens fed the organic selenium as Sel-Plex, a selenized yeast, had elevated GPX activity in both blood and liver in a thermoneutral environment and after heat distress. More importantly, the ability to reduce the oxidized glutathione (GSSG to 2 GSH) was enhanced and facilitated by maintenance of glutathione reductase activity. Organic selenium-fed chickens were less affected by mild heat distress than inorganic selenium-fed chickens, and this assessment was based upon less induction of heat shock protein 70 (hsp70) in organic selenium-fed chickens. Our results clearly show that heat distress, a potent inducer of oxidative stress and hsp70, can be partially ameliorated by feeding organic selenium. We attribute this observation to an enhanced GSH-GPX antioxidant system in organic selenium-fed chickens.

Demasculinization of male Japanese quail by prenatal estrogen treatment

Abstract Genetic male Japanese quail were administered sex hormones or the oil vehicle on Day 10 of incubation and were caponized 3 weeks after hatching. As adults, the capons were injected with testosterone propionate daily for 2 weeks and then were tested for masculine sexual behavior in response to sexually receptive females. Males that had received as little as 2 μg of estradiol-17β in ovo failed to exhibit the head grabbing and mounting typical of the normal masculine sexual response to females. In a second experiment, this demasculinization was produced by prenatal treatment with 2 μg of estradiol-17α, estrone, estriol, or diethylstilbestrol, but not by this quantity of testosterone. These data suggest that an estrogen is the agent of behavioral demasculinization in the normal female, and that endogenous testosterone poses no difficulty for proper sexual development in the normal male.

Agonistic behavior and neurochemistry in grouped Japanese quail

Aggressive behavior and whole brain neurochemistry were measured in stable and unstable pairs of male Coturnix coturnix japonica. Aggressive pecking peaked on day 5 of the daily regrouping regime and returned to a basal level on day 14. Aggressive behavior was associated with increased brain norepinephrine (NE), dopamine (DA), and acetylcholinesterase (AChE) in unstable pairs. Habituation (12-15 days) and DA response to daily regrouping and inanition were inversely related in unstable and stable pairs respectively. Normal whole brain NE increases were attenuated in unstable pairs.

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

Abstract 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.

Isolation of a Reovirus from Poult Enteritis and Mortality Syndrome and Its Pathogenicity in Turkey Poults

SUMMARY. 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 ≤ 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 ≤ 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 ≤ 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.

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.

Effect of dietary lead on reproductive performance in Japanese quail, Coturnix coturnix japonica

Abstract Japanese quail received dietary lead at levels ranging from 1 to 1000 μg/g of feed from hatching through 12 weeks of age. Levels of lead which did not cause depressed growth rates, anemia, or any other overt signs of chronic plumbism caused a decrease in reproductive capacity in the females. This decrease in reproductive capacity appeared to be related to impaired calcium metabolism.

D-xylose absorption as a measurement of malabsorption in poult enteritis and mortality syndrome

Abstract Severe wasting of body tissues, diarrhea, high morbidity and mortality, and stunting are all characteristics of poult enteritis and mortality syndrome (PEMS). The wasting of musculature and loss of nearly all adipose tissue suggested that even though the PEMS-infected poults were eating some feed, nutrient intake was not sufficient to meet body requirements for maintenance and growth. Because epithelial cells in the gastrointestinal tract appeared to be a target of the undefined etiological agent (or agents) that causes PEMS, a study was conducted in which PEMS-infected poults were evaluated for malabsorption through 3 wk of age. D-Xylose, a poorly metabolized pentose, was given per os as a bolus, and blood samples were obtained from the ulnar vein in the wing of control and PEMS-infected poults over a 3-h period to estimate intestinal absorption. D-Xylose absorption in control poults peaked 30 to 60 min after the oral treatment, similar to results reported earlier. The PEMS-infected poults did not show a peak in absorption. The PEMS-infected poults showed significant delays in D-xylose absorption at 4, 7, and 11 d after PEMS challenge. The severe malabsorption and metabolic deficiency problem associated with PEMS was postulated to be a direct effect of the undefined infectious agent or agents that cause the disease.

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.

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

Abstract 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.