Influence of a propionic acid feed additive on performance of turkey poults with experimentally induced poult enteritis and mortality syndrome.

Poult enteritis and mortality syndrome (PEMS) has multiple etiological agents associated with its occurrence, including two viruses and at least three Escherichia coli isolates. Myco Curb (MC) contains organic acids and is used as a feed additive to inhibit growth of many bacteria and toxin-producing molds but not viruses. Studies evaluating the influence of MC on BW, feed conversion, and mortality indicate that turkey poults tolerate MC at 1.25% but not 2.50%, but higher MC content in feed provides greater suppression of growth of bacterial isolates commonly associated with PEMS. In two PEMS experiments, 1.25% MC was blended into poult starter feed and was maintained in the feed for the duration of the 3-wk experiments. In these experiments, 1-d-old commercial poults were placed into battery brooders and were given turkey starter feed and water ad libitum. At 6 d posthatch, PEMS-designated poults were given a 1-mL oral gavage of a 10% suspension of feces from PEMS-infected poults. BW depression due to PEMS was not alleviated by MC, although there was less variation in mean BW of the MC-fed poults, and there was a highly significant reduction in mortality (68% in PEMS-exposed with MC vs. 32.5% in PEMS-exposed without MC). The reduction in mortality in the MC-fed poults was attributed to decreased bacterial content of the gut and to maintenance of packed cell volume and hemoglobin content. It was concluded that MC might be a potential nutritional intervention during PEMS.

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

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.

Influence of BioChrome on the response of metabolic hormones in PEMS-infected poults.

Poult enteritis and mortality syndrome (PEMS), a disease that affects turkeys between 7 and 28 d of age, causes a severe inflammation of the intestinal tract and is characterized in poults by severe diarrhea, high morbidity, mortality, and stunting. The PEMS-associated mortality and growth depression is related to malabsorption and decreased metabolic activity caused, in part, by a possible insulin deficiency or insensitivity. Insulin receptors are stimulated by the glucose tolerance factor (GTF) that incorporates Cr. Body Cr deficiency can be exacerbated by dietary deficiency and by increased excretion due to stress associated with a diarrheal disease such as PEMS. BioChrome (BC) contains natural, preformed GTF, the bioactive form of Cr. Experiments were conducted in which BC was blended into poult starter feed at 400 ppb during the first 21 d posthatch. Body weights were determined at 1, 7, 14, and 21 d of age, and weekly feed conversions were calculated for each treatment group (control, BC, PEMS, and BC+PEMS). At 6 d post-hatch, each PEMS-designated poult was given a 0.1-mL oral gavage of a 10% suspension of feces from PEMS-infected poults. Blood samples were taken via cardiac puncture from four birds per treatment group at 7, 10, 14, 17, and 21 d of age. Radioimmunoassays were conducted for plasma insulin, glucagon, thyroxine (T4), and triiodothyronine (T3). Plasma insulin levels were depressed in PEMS-infected poults from Days 10 through 17, but plasma glucagon levels in the PEMS-infected poults were significantly elevated at 14 and 17 d, after which they returned to control levels in both of the PEMS-infected groups. The T3 and T4 levels were depressed through Day 21 in PEMS-infected poults, but with BC treatment these blood hormone levels rebounded by Day 21. Body weights of PEMS-infected poults were increased significantly by the BC treatment but not to the level of noninfected controls.

Hypothermia, hypoglycemia, and hypothyrosis associated with poult enteritis and mortality syndrome.

A metabolic dysfunction contributes to the poor performance and mortality associated with Poult Enteritis and Mortality Syndrome (PEMS). Within 2 d after contact-exposed poults were removed from the presence of PEMS-infected poults and returned to their respective treatment rooms to infect experimental poults, the experimental poults began to huddle together and show signs of the disease. When separated from the huddle, body temperatures of exposure poults were depressed significantly. Body temperatures decreased progressively through 8 d after exposure with a maximum depression of 2 C and returned to a normal level at 18 d after PEMS exposure. Similar decreasing patterns in serum glucose, inorganic phosphorus, triiodothyronine, and thyroxine were observed, with maximum decreases in these serum constituents being found between 8 and 13 d after PEMS exposure. There were significant correlations among decreasing body temperatures, decreasing serum constituents, and mortality in the PEMS-exposed poults. Daily mortality rates associated with PEMS began at 6 d and peaked at 9 d after PEMS exposure. Mortality rates decreased from 9 to 15 d after experimental PEMS exposure. Depressions in serum constituents, body temperature, and increased mortality rates did not coincide with decreased feed intake associated with PEMS. Therefore, it was concluded that the agent(s) causing PEMS may have a direct effect on energy metabolism in afflicted poults.

Effect of litter moisture and brooding temperature on body weights of turkey poults experiencing poult enteritis and mortality syndrome.

Studies were conducted to determine the influence of the interactions among litter moisture (high [HiM]> or =40% vs low [LoM]< or =20%), brooding temperature (high [HiB] = 38 C vs normal [NrB] = 34 C), and development of poult enteritis and mortality syndrome (PEMS) as indicated by body weights, relative weights of lymphoid organs, and mortality in Control [C] vs Infected [I] groups. There was a significant interaction between litter moisture and brooding temperature that had a significant influence on BW. The brooding temperature main effect was not significant, but there was a significant litter moisture effect on BW. Body weights were suppressed by PEMS infection, but infected poults brooded at HiB on LoM had significantly greater BW than those brooded at NrB and HiB on HiM. Main effects showed that there were significant litter moisture- and brooding temperature-mediated responses for BW. Relative weights of lymphoid organs revealed significant disease main effects but no effect due to brooding temperature and litter moisture. There was a significant effect of disease and brooding temperature with regard to mortality. The results from this study suggest that litter moisture influences productivity and mortality associated with PEMS, but brooding temperature has the greatest influence on PEMS-associated mortality. Therefore, higher brooding temperature for turkey poults being placed into a facility where they may be at risk for PEMS exposure is recommended.

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.

Principles of ex ovo competitive exclusion and in ovo administration of Lactobacillus reuteri.

The data that have been presented indicate that the in ovo use of competitive exclusion (CE) agents is feasible for both chickens and turkeys. However, there are many pitfalls that await the use of in ovo application of CE agents, including the use of nonspecies-specific intestinal microbes and the use of harmful proteolytic, gas-producing and toxin-producing intestinal microbes. Of the potential CE agents that have posthatch application, only Lactobacillus reuteri has been shown to be safe and effective in terms of not affecting hatchability and in having a prolonged effect in the hatched chick or poult. Lactobacillus reuteri administration in ovo increases its rate of intestinal colonization and decreases the colonization of Salmonella and Escherichia coli in both chicks and poults. Additionally, mortality due to in-hatcher exposure to E. coli or Salmonella is reduced with in ovo L. reuteri. Use of antibiotics in ovo may preclude the use of co-administered CE agents, but Gentamicin and L. reuteri are a compatible mixture when administered in ovo in separate compartments. Nevertheless, the intestinal morphology can be affected by both the CE agent and by antibiotics. Lactobacillus reuteri both in ovo and ex ovo will increase villus height and crypt depth, and Gentamicin in ovo causes a shortening and blunting of the villus. Both Gentamicin and L. reuteri in ovo suppress potentially pathogenic enteric microbes, but with diminished antibiotic effects shortening and blunting of the intestinal villi does not correct itself. Goblet cell numbers increase significantly on the ileum villus of chicks treated with Gentamicin in ovo, and this is presumably due to the increase in potentially pathogenic bacteria in the intestinal tract. Diminishing antibiotic effects posthatch would then negatively affect the absorption of nutrients and reduce growth at least in a transitory manner. Thus, L reuteri administration in ovo singly or in combination with Gentamicin followed by L reuteri via drinking water or feed appears to have potential to control many enteric pathogens in poultry. Additional work in the use of in ovo CE cultures is mandated because there is a world-wide movement to reduce antibiotic use in poultry due to increased microbial resistance to antibiotics. Use of naturally occurring intestinal bacterial cultures, either in mixed culture or as single well-defined cultures, has potential for immediate use in the poultry industry.

Characterization of two Escherichia coli isolates associated with poult enteritis and mortality syndrome.

Two colonial types (1 and 2) of Escherichia coli are represented predominantly in cultures isolated from turkey poults with poult enteritis and mortality syndrome (PEMS). Biotype codes determined using two systems (BBL: 36570 and 34560 for colony types 1 and 2, respectively; API-20E: 5144572 and 5144512 for colony types 1 and 2, respectively) clearly establish these organisms as E. coli. These isolates were not clearly divergent from the general profile for E. coli, but colony type 2 differs from colony type 1 with regard to its negative reactions for ornithine decarboxylase and the fermentation of dulcitol, rhamnose, sucrose, and melibiose, suggesting that it is atypical. Colony type 1 is nonserotypable and nonmotile, whereas colony type 2 is serotyped as O136: motile because it has H antigens associated with flagella. Capsular antigens were not found, but thin capsules were seen on cells from both colony types in stained preparations. Cultural morphology was different with colony type 1 having a circular, mucoid, raised morphology and colony type 2 having an irregular, flat, rough morphology. Colony type 1 has a doubling time at 37 C of about 20 min, whereas colony type 2 doubles in 30 min. Furthermore, colony type 1 is a potent colicin producer, but colony type 2 is not a colicin producer. Both E. coli isolates have resistance profiles for multiple antibiotics. Each strain responds to third generation fluoroquinolone antibiotics by changing their biotypes and become resistant after culturing once in their presence. These E. coli are proposed as possible etiological links in the complex series of events that take place in poults susceptible to PEMS.

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)

Photoperiod and seasonal influences on the growth of turkey hens.

1. The influence of photoperiod and time of year on the growth of hen turkeys was investigated. 2. Photoperiod treatments consisted of computer simulations of day lengths which occur naturally in the spring and autumn of the year. Both photoperiod treatments were given to hens in the autumn and spring. 3. Data were collected for growth evaluations at 2- to 4-week intervals to 16 weeks of age. No significant season X photoperiod interactions occurred. 4. The spring trial resulted in greater body weights and better food conversions (food/gain) than the autumn trial. 5. Simulated autumn daylengths resulted in greater body weights and improved food efficiency at 16 weeks of age compared with simulated spring daylengths. 6. The pattern of growth (period changes) was influenced by season, but not photoperiod. 7. Season and photoperiod both have important and independent influences on the growth of the turkey hen.

Abnormal feathering of chicks caused by scirpenol mycotoxins differing in degree of acetylation.

Graded levels of the Fusarium mycotoxins, scirpentriol (STO), 15-monoacetoxyscirpenol (15-MAS), 4,15-diacetoxyscirpenol (4,15-DAS), and 3,4,15-triacetoxyscirpenol (TAS), were fed to chicks until 3 wk of age. The primary wing feathers, which were scored visually on a scale of 1 to 5 using a newly created scoring scheme, were altered in a dose-related fashion by 15-MAS [minimum effective dose (MED) = .5 microgram/g diet], 4,15-DAS (MED = 2 micrograms/g), and STO (MED = 4 micrograms/g) but not by TAS (MED greater than 8 micrograms/g). The minimum growth inhibitory doses were 2 micrograms/g for STO, 15-MAS, and 4,15-DAS and 8 micrograms/g for TAS. The main alteration of the feathers was a frayed and missing web on the medial side of the distal half of the feather. The shafts of the feathers tended to have an accentuated medial curve. These results imply that the feather alterations associated with corn and feed infested with Fusarium spp. might be caused by trichothecene mycotoxins such as the scirpenols.

Relationship between duration and intensity of environmental light on the growth performance of male turkeys.

In each of two trials a 2 x 2 factorial arrangement of treatments was used to evaluate the growth response of tom turkeys to environmental light. The main experimental light treatment factors were: daylength [23 h light (L):1 h dark (D) vs. 8 h L:16 h D] and light intensity (10.8 lx vs. 108 lx). There were 100 toms in each treatment; all birds were in closed confinement floor pens exposed to artificial light only. Data were collected for growth performance evaluations at 2 to 4-wk intervals to 22 wk of age. No significant daylength x intensity interactions occurred in the study. No consistent effect of daylength or light intensity on body weight occurred. Light intensity had no significant effect on feed conversion but 23 h L:1 h D significantly (P less than or equal to .01) improved feed conversion from that in the 8 h L:16 h D treatment at 18 and 22 wk of age. This occurred in both trials. Neither the daylength nor the light intensity treatment effects differed with regard to livability or to incidence of leg disorders. Testicular development at 22 wk of age of birds in the two intensity treatments was similar but testes were significantly (P less than .01) larger in the 23 h L:1 h D treatment than the 8 h L:16 h D treatment. Percentage of breast yield was not influenced significantly by the daylength or intensity treatments but the amount of abdominal fat was significantly greater in the 8 h L:16 h D group than the 23 h L:1 h D group. From the results of this study it seems clear that daylength can have an important impact on the growth performance of tom turkeys whereas variations in light intensity ranging from 10.8 to 108 lx generally resulted in negligible differences in response.

Carotenoid composition of serum and egg yolks of hens fed diets varying in carotenoid composition.

High performance liquid chromatography of yolks of hens fed a diet based on yellow corn, alfalfa, and soybeans revealed over 20 cartenoids. Lutein, lutein monester, lutein diester, 3'-oxolutein, cryptoxanthin, zeaxanthin, beta-carotene, and zeacarotene were identified by their retention times, visible absorption spectra, behavior on saponification, and their presence or absence when lutein was the primary carotenoid fed. Three weeks after placing the hens on a white corn-soy-based diet supplemented with lutein (20 micrograms/g diet), cryptoxanthin, zeaxanthin, and zeacarotene were undetectable in the yolk and lutein, lutein monoester, lutein diester, and 3'-oxolutein assumed new equilibrium concentrations. The data imply an esterification pathway and an oxidative pathway in laying hens for the metabolism of hydroxycarotenoids. Consideration of the concentrations and ratios of lutein and its metabolites in serum and yolk suggest a nonovarian site for the metabolism of lutein in laying hens.

Plasma corticosterone in hemorrhaged Japanese quail after microwave irradiation in ovo.

1. Sexually immature male and female Japanese quail were divided within each sex into three treatment groups: hemorrhaged by jugular puncture; immobilized for 2 min, but not hemorrhaged (shams); and neither immobilized nor hemorrhaged (controls). 2. Hemorrhage resulted in increased plasma corticosterone levels in both sexes. Corticosterone levels in shams were higher than in controls. 3. In another experiment, Japanese quail eggs were irradiated during incubation with 2.45 GHz CW microwave radiation. Nonirradiated eggs were incubated under identical conditions without irradiation. After hatching, juvenile males and females were hemorrhaged. 4. After hemorrhage, irradiated males had higher plasma corticosterone levels than nonirradiated males. No effect of irradiation on females was found. 5. The results of these two experiments indicate that male quail respond to blood loss with increased adrenocortical activity and that this response is modified in male quail after irradiation with microwaves during embryogeny.

Hematological effects of ethyl methanesulfonate, paraquat and phenylhydrazine in Japanese quail.

1. Juvenile Coturnix coturnix japonica males were injected intravenously with 2, 20 or 200 mg ethyl methanesulfonate (EMS)/kg body wt; 0.2, 2 or 20 mg paraquat (PARA)/kg body wt; or 0.6, 6 or 60 mg phenylhydrazine (PHZ)/kg body wt; and hematologic variables were measured at 0 (non-injected), 24 and 72 hr post-injection. 2. EMS, PARA and PHZ-induced hemolytic anemia began within 24 hr post-injection. 3. Recovery from anemia began within 72 hr post-injection of EMS or PARA, but PHZ injected quail continued to show a marked anemia at that time. 4. EMS and PARA induced lymphocytopenia, monocytopenia and heterophilia, while PHZ induced lymphocytosis, monocytopenia and heteropenia after injection. 5. These results suggest that the anemia induced by EMS and PARA was dissimilar from that induced by PHZ, that all chemicals affected leukopoiesis and that Japanese quail can mount a marked recovery from the hematologic affects of PARA, a widely used herbicide, in a short interval after intoxication.

Egg production in four generations of paired Japanese quail.

Four generations of Japanese quail were hatched in succession starting with the progeny of an Athens Randombred quail colony. In each generation quail were maintained in cages as male-female pairs. The photoperiod was 16 hr of light per day with feed and water available ad libitum. From 6 to 20 weeks of age mortality, egg production, fertility, hatchability, and progeny livability were improved over previously published reports of reproduction in colony cages. Mortality decreased while age at 50% hen-day production, total number of eggs produced, and hatchability increased from the 1st to the 4th generation. This information may be of interest to researchers and commercial producers of Japanese quail.

Reproduction of Japanese quail after microwave irradiation (2.45 GHz CW) during embryogeny.

Japanese quail (Coturnix coturnix japonica) embryos were irradiated continuously in ovo with 2.45-GHz continuous wave radiation during the first 12 days of embryogenesis at an incident power of 5 mW/cm2 and a specific absorption rate of 4.03 mW/g. The internal temperature of irradiated and nonirradiated (sham) eggs was 37.5 +/- 0.3 degrees C, which is the optimum temperature for incubating quail eggs. At 35 days after hatching irradiated and sham-irradiated males were paired with irradiated or sham-irradiated females and daily records of reproductive performance were collected through 224 days of age. Progeny were hatched from each of the male-female pairs, and progeny reproductive performance was measured from 35 through 168 days of age. Hatchability was not affected by irradiation during embryogeny. Mortality after hatching, egg production, egg weight, fertility, hatchability of eggs produced, and reproductive performance of the progeny were not affected by irradiation during embryogeny. These observations indicate that irradiation of quail embryos with low-level microwave radiation does not affect the reproductive capacity of the hatchlings or of progeny produced from quail irradiated during incubation.

Leukocyte numbers in hemorrhaged Japanese quail after microwave irradiation in ovo.

1. Coturnix coturnix japonica eggs were exposed to 2.45-GHz continuous wave microwave radiation at an incident power density of 5 mW/cm2 (and a specific rate of 4 mW/g) during the first 12 days of embryogeny. After hatching, hematological changes in response to an acute hemorrhage were measured in exposed and nonexposed (control) juveniles of both sexes. 2. Exposure did not affect erythroid cell numbers either before or after hemorrhage. 3. Exposure affected the recovery of lymphocyte and heterophil numbers after hemorrhage, but the effect was sex-limited. 4. These data indicate that microwave irradiation during embryogeny in ovo affects the ability of Japanese quail to recover from an acute and voluminous hemorrhage and that these radiation effects are sex-limited and consistent with a previous report.

Leukocyte numbers during the humoral and cell-mediated immune response of Japanese quail after microwave irradiation in ovo.

1. Coturnix coturnix japonica eggs were exposed to 2.45-GHz continuous wave microwave radiation at an incident power density of 5 mW/cm2 (SAR = 4 mW/g) during the first 12 days of embryogeny. After hatching, leukocyte differential changes were measured in response to an injection with Alectoris graeca chukar red blood cells (CRBC) and in response to a phytohemagglutinin (PHA) injection in irradiated and nonirradiated (sham) quail of both sexes. 2. Microwave irradiation did not affect anti-CRBC hemagglutinin titers, PHA-evoked dermal swelling or leukocyte numbers and percentages. 3. In both the irradiated and sham irradiated males, lymphocyte percentages decreased while heterophil percentages increased after CRBC or PHA injection. 4. In ovo irradiation with microwaves did not alter the time course of either a humoral immune response or a cell-mediated immune response in Japanese quail.

Hematology of Japanese quail selected for high or low serum corticosterone responses to complex stressors.

Blood was collected from random-bred male Coturnix coturnix japonica and from quail selected genetically for high or low serum corticosterone responses to complex stressors after chronic exposure to short daily photoperiods and after exposure to long photoperiods. When compared to the low response quail, high response quail exhibited increased mean cellular hemoglobin values, reticulocyte numbers and heterophil percentages, and decreased monocyte and eosinophil numbers after exposure to long photoperiods. The data indicate that these corticosterone response lines can be partitioned by their hematological responses to photoperiodic manipulation.