G. B. Havenstein

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.

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.

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.

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

Abstract 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.

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.

Alterations in the Lymphocytic and Mononuclear Phagocytic Systems of Turkey Poults Associated with Exposure to Poult Enteritis and Mortality Syndrome

In vivo and in vitro mononuclear phagocytic system functions, expression of lymphocyte subset cell surface markers in the thymus and bursa of Fabricius, and lymphocyte subset dynamics during the course of poult enteritis and mortality syndrome (PEMS) were examined. PEMS is an acute, transmissible, infectious intestinal disease accompanied by high mortality and morbidity. The etiology of this multifactorial disease remains to be elucidated; however, turkey coronavirus was initially assumed to be one of the primary agents involved. Further investigation demonstrated that turkey coronavirus was not always detectable in poults exhibiting PEMS symptoms, and, thus, PEMS poults began to be identified as positive or negative for turkey coronavirus. In each trial, uninfected hatchmate controls were compared with turkey poults that were contact exposed to PEMS poults at 7 days of age. Following intravenous inoculation, control poults cleared Escherichia coli from their circulation by 60 min, whereas viable E. coli were still present in the circulation of PEMS poults at 60 min postinoculation. Inflammatory response measured by Sephadex-elicited abdominal exudate cell recruitment and the adherence potential of abdominal exudate cells was not significantly different between uninfected and PEMS poults. The percentage of glass-adherent abdominal exudate macrophages was higher in PEMS poults. However, the ability of these macrophages to phagocytize sheep red blood cells and the average number of sheep red blood cells per phagocytic macrophage were both lower compared with uninfected controls. CD4+ expression in thymic tissue of PEMS poults at 9 days postinfection was significantly lower. The CD4+:CD8+ lymphocyte ratio in peripheral blood leukocytes from coronavirus-negative PEMS poults was lower than that from both uninfected and coronavirus-positive PEMS poults at 14 days postinfection. In the spleen, the CD4+:CD8+ lymphocyte ratio was higher in coronavirus-positive PEMS poults as compared with the other treatments. In conclusion, immune system dysfunction in PEMS is associated with impaired mononuclear phagocytic system function and alterations in lymphocyte populations.

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

Abstract 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.

Farm-Scale Evaluation of Ozonation for Mitigating Ammonia Concentrations in Broiler Houses

Abstract This study evaluated the effectiveness of in-house ozonation within the public health standard limit (0.1 parts per million [ppm]) for mitigating ammonia (NH3) concentrations inside commercial broiler houses. The project was conducted in four identical tunnel-ventilated houses. Two houses served as treatment and the other two served as control units. The experiment was replicated in five consecutive flocks. Except for ozonation treatment, all other operational parameters including feed, broiler strain, age and number of broilers, and ventilation system were the same among four houses. NH3 and carbon dioxide (CO2) concentrations in the treatment and control houses were measured for a minimum of 48 hr/week throughout the five flocks of 8 or 9 weeks each. The gas measurements were conducted using portable multigas units (PMUs). House temperatures were recorded with data loggers in each flock. Comparison of temperatures and CO2 concentrations among houses indicated no significant differences in ventilation rates among treatment and control houses in any of the five flocks. As a result, comparisons of NH3 concentrations inside houses were used to evaluate the effectiveness of house ozonation for NH3 emission mitigation. Statistical test of mean NH3 concentrations for each flock separated by house indicated that the house-to-house variation was significantly smaller than the flock-to-flock variation. There was a substantial variation in NH3 concentrations across different flocks, but no house had consistently higher or lower mean NH3 concentrations than any other. Evaluations for differences in mean NH3 from week to week, between treatment groups, and differences in week-to-week variations between treatment groups suggested that ozone effect was not uniform for each week and the effect was not statistically significant for any week. Tests of overall ozone treatment effect and treatment-week interaction indicated there was no difference in mean NH3 between the control and ozone treatment groups (P = 0.25), nor was the week effect different for control and treatment groups (P = 0.46). The results of this field evaluation indicate that there was no statistical evidence to suggest that the ozone treatment has any effect on average NH3 concentrations in these chicken houses.

Changes in commercial laying stock performance, 1958-2011: thirty-seven flocks of the North Carolina random sample and subsequent layer performance and management tests

Thirty-seven layer performance tests have been conducted at North Carolina State University during the past 53 years. Originally established as the North Carolina Random Sample Layer Test (NCRSLT), all of the test flocks have been hatched and housed at the Poultry Unit of the North Carolina Department of Agriculture and Consumer Services Piedmont Research Station at Salisbury, North Carolina. In 1988, the NCRSLT name was changed to the North Carolina Layer Performance and Management Test (NCLP&MT) reflecting changes in the testing procedures to include the evaluation of management practices used by commercial egg producers. Strain testing and evaluating the relative egg production of commercially available egg production stocks began in 1911, and the number of such Random Sample Tests in North America peaked at 23 in approximately 1968. The mission for the NCRSLT to provide an unbiased evaluation of the overall performance of strains, evolved to include the effects of various housing and husbandry practices on the performance of the genetic stocks entered into the test. Test results have been distributed to the industry throughout the USA as well as to producers in 22 other countries throughout the world. In addition, the internet site for the NCLP&MT http://poultry.ces.ncsu.edu/layer-performance/ allows the distribution of the results to many other interested university and government officials. This review of the first 37 North Carolina layer tests shows continuing improvements in egg production, reduction in body weight and feed consumption, increases in egg weight and feed conversion, improvements in liveability, and an improvement in egg quality from the commercially available white and brown egg strains. These changes have continued throughout the 50+ year history of the tests, and the changes observed have been brought about primarily by poultry breeding companies applying quantitative genetics for the improvement of the layer stocks used worldwide.

Genetic Control of Embryonic Cardiac Growth and Functional Maturation in Turkeys

Turkey experimental lines E (selected 44 yr for increased total egg production) and F (selected 38 yr for increased 16-wk BW) were mated reciprocally with the randombred control lines from which they were derived (RBC1 and RBC2, respectively), and the pureline and reciprocal cross poults were compared for their BW, heart weight, heart rates, myocardial glycogen and lactate concentrations, and plasma creatine kinase (CK) and lactate dehydrogenase (LDH) activities. The CK and LDH were used as indicators of cardiac insufficiency. Orthogonal contrasts of the data from the pureline and reciprocal cross data were used to estimate additive genetic effects, reciprocal effects (confounded maternal and sex-linked effects), and heterosis for each of the traits measured. Long-term selection for increased egg production in the E line has reduced embryo heart weight and has altered the energy metabolism of the myocardium. The differences in energy metabolism may be due to the more rapid heart rates. Conversely, long-term selection for increased 16-wk BW has significantly decreased the heart rate of F line embryos and has not changed the weight of the heart relative to the BW until the embryo has passed through the plateau stage. The F line embryos show a different energy metabolism that relies much more on gluconeogenesis. Embryo deaths occur more frequently in turkey embryos when the energy metabolism of the myocardium shows elevated glycogen to lactate ratios as it did in the pure E and F lines.