Rapid decrease of the peripheral deiodination of thyroxine in malabsorption syndrome in artificially inoculated broilers

Thyroid function of broilers inoculated with the intestinal homogenate from birds from a field case of malabsorption syndrome was investigated during the first 2 days postinoculation. In one experiment, different amounts of the inoculum were applied to see if there exists a dose-response relationship. As early as 3 hours after inoculation, there was a significant drop in the serum level of triiodothyronine and in the activity of the liver 5'-deiodinase (type I). Type II deiodinase activity was less impaired. A minimum of 0.3 ml of inoculum was effective, whereas 0.05 ml of the same homogenate elicited a significant (P less than 0.01) drop in liver deiodinase activity. These findings underline the importance of thyroid impairment in the pathogenesis of malabsorption syndrome.     

Effect of infectious stunting syndrome on the immunocompetence of broilers

Immune responses and liveweights of broilers affected with the stunting syndrome (group C) were compared with those of unaffected birds from the same premises (group B) and normal control broilers of the same genetic origin (group A). Measurements of cell-mediated immunity were made using the phytohaemagglutinin (PHA) intradermal test and those of humoral immunity by antibody response to sheep red blood cells. Weekly observations were made of birds aged from two to eight weeks. Throughout the investigation the weekly mean weight of affected birds was very significantly lighter (P less than 0.001) than that of unaffected and control birds. From the second to the sixth week, wing web PHA reactions in group C were very significantly less than those in groups B or A (P less than 0.001), and during the seventh and eighth week wattle PHA reactions were significantly less in group C than those in group B (P less than 0.02). No significant differences were detected between the three groups in humoral immunity; the complete, IgG and IgM, antibody levels being closely similar. The significance and possible practical applications of these findings are discussed.     

Echocardiographic study of pulmonary hypertension syndrome in broiler chickens

Echocardiography was used to study cardiovascular structure and function during the development of pulmonary hypertension syndrome (PHS) in broiler chickens. Body weight-normalized right and left ventricular diameters at both end-diastole (RVDD, LVDD) and end-systole (RVDS, LVDS) were determined weekly in broilers reared under either normobaric (altitude, 96.7 m) or hypobaric conditions (simulated altitude, 2900 m) until 5 wk of age. Hypobaric-exposed broilers had larger RVDD at 3 and 4 wk of age and larger RVDS at 3, 4, and 5 wk of age. Hypobaric-exposed broilers also had larger LVDD at 2, 3, 4, and 5 wk of age and larger LVDS at 4 wk of age. Right (RVFS) and left ventricular fractional shortening (LVFS) were smaller in hypobaric- vs. normobaric-exposed broilers at 3, 4, and 5 wk of age and at 4 wk of age, respectively. Among hypobaric-exposed birds, PHS-positive (+) broilers had larger RVDD and RVDS than PHS-negative (-) broilers on week 3 and on weeks 1 and 3 after hypobaric exposure, respectively. PHS-positive (+) broilers also had smaller RVFS on week 1 after hypobaric exposure. Electrocardiographic and post-mortem data indicated that PHS+ broilers also developed right ventricular hypertrophy when compared with PHS-negative (-) broilers. These results are consistent with the hypothesis that PHS develops as a result of pulmonary hypertension and cardiac overload and suggest that PHS+ broilers have a greater and more persistent reaction to hypoxia than PHS- broilers.     

The effects of age, route of exposure, and coinfection with infectious bursal disease virus on the pathogenicity and transmissibility of chicken anemia agent (CAA)

Specific-pathogen-free (SPF) chickens were inoculated with several different concentrations of chicken anemia agent (CAA) by the intra-abdominal, intratracheal, or oral routes. Based on lowered hematocrit values, the birds were most susceptible to CAA introduced by the intra-abdominal route. When SPF chickens were infected with infectious bursal disease virus (IBDV) at 1 day of age, they remained susceptible to CAA up to at least 21 days, whereas birds inoculated with CAA alone were susceptible only at 1 day of age. Infectious bursal disease virus introduced at 1 day of age also increased the susceptibility of birds to contact infection with CAA and resulted in increased mortality rates in CAA inoculates. The response of SPF birds to CAA infection varied following exposure at 1 day of age to two different strains of IBDV (STC and Variant-E). Chicken anemia agent contacts and inoculates infected with the Variant-E strain were affected 1 week earlier by CAA than by STC inoculates, as evidenced by depressed hematocrits. However, the total number of birds affected was similar for both the Variant-E and STC-inoculated chickens. Commercial broiler chickens inoculated at 1, 7, 10, and 14 days of age by non-parenteral routes with CAA or a combination of CAA and IBDV had mean hematocrits that were lower than controls. Several CAA-inoculated birds were considered anemic, with hematocrit values of 25 or less, while uninoculated birds remained within normal ranges.     

Changes in hematological, blood gas, and serum biochemical variables in broilers during exposure to simulated high altitude.

One-day-old broilers were reared until 35 days of age at both natural low (100 m) and simulated high altitude (2133 m) to assess the incidence and development of ascites syndrome. Clinical measurements were conducted at 7, 14, 21, 28, and 35 days of age. Birds reared at 2133 meters exhibited significantly (P less than or equal to 0.05) reduced body weights at 7 through 28 days of age. Total serum calcium and biochemical enzyme activities were found to be altered at 35 days of age. In addition, the high-altitude group had significantly (P less than or equal to 0.05) higher erythrocyte counts, hematocrits, and hemoglobin at 14, 21, 28, and 35 days of age and higher serum inorganic phosphorus at each weekly sample time than birds at the low altitude. Total mortality was 20.3% at 2133 meters and 4.6% at 100 meters. The incidence of ascites syndrome in the high-altitude group ranged from 16.6% to 61.1% during the 5-week experimental period.     

Effects of Early Feed Restriction on Performance and Ascites Development in Broiler Chickens Subsequently Raised at Low Ambient Temperature

The objective of this study was to examine the effectiveness of early-age growth limitation, achieved through feed restriction (FR), as a means of reducing ascites mortality in broiler chickens exposed to low ambient temperatures. Feed restriction was applied to broilers from 5 to 11 d of age so as to reduce their weight gain to about 40% of that of control broilers that were fed ad libitum (AL). At the age of 21 d the chickens were exposed to a temperature of 15°C, which induced ascites. By 46 d of age, ascites incidence and mortality in the feed-restricted birds were reduced to 15.79 vs. 36.84% and 7.89 vs. 26.32%, respectively, compared with those in the controls (P < 0.05). After feed restriction was stopped, the FR chickens had accelerated weight gain and improved feed conversion ratio from 11 to 18 d of age (P < 0.05), and by 46 d they had achieved the same body weight as the AL birds. Ascitic broilers had smaller relative breast muscle and spleen weights than those of the healthy broilers at 46 d (P < 0.05). However, the relative weights of lung, heart, and liver and the right ventricle weight per total ventricle weight (RV:TV) ratios were greater in ascitic broilers (P < 0.05). At age 37 d, when ascites had developed but not yet caused mortality, the ascitic broilers had lower plasma concentrations of the thyroid hormones thyroxine and triiodothyronine, and higher hematocrit values (P < 0.05) in comparison with the healthy ones. Ascitic birds also had lower oxygen consumption at 6 wk (P < 0.05), which agrees with information that the terminal stage of the ascites syndrome can be characterized by low oxygen consumption. We concluded that the early-age feed restriction reduced ascites incidence and mortality and prevented reduction of the thyroid hormone concentrations in male broilers reared at low ambient temperature from the age of 3 wk onward.     

氨气对肉鸡生产性能、血液常规指标和腹水症发生率的影响

为探讨氨气对肉鸡生产性能、血常规指标和腹水症发生率的影响。试验选择240只1日龄AA肉公鸡,随机分成4个处理组,每个处理组设6个重复,每个重复10只鸡。各处理组试验肉鸡分别饲养在4个独立的、但环境可控制的实验舱内。4个环控仓氨气浓度设计:0～3周龄分别为0、13、26mg/kg和52mg/kg;3～6周龄分别依次调整为0、26、52mg/kg和80mg/kg。结果表明:氨气浓度对0～3周龄肉鸡的日增重、日采食量和死亡率均无显著影响(P>0.05),但52mg/kg氨气组可显著降低饲料转化效率(P<0.05);在3～6周龄,80mg/kg氨气组可显著降低肉鸡的日增重和日采食量(P<0.05),饲料转化率和死亡率在数值上随氨气浓度的提高有上升趋势,但差异不显著(P>0.05)。氨气浓度对3周龄和6周龄肉鸡血常规,6周龄肉鸡心脏指数和腹水发生率均无显著影响(P>0.05),但红细胞数量、红细胞压积和红细胞平均体积随氨气浓度的提高在数量上有所增加。高浓度氨气(80mg/kg)有诱导肉鸡腹水症发生的趋势。综合考虑氨气浓度和肉鸡生产性能变化趋势,现代肉鸡在0～3周龄舍内氨气浓度应不超过13mg/kg,在3～6周龄氨气浓度应不超过20mg/kg。     

The effect of dietary l-carnitine supplementation on pulmonary hypertension syndrome mortality in broilers exposed to low temperatures

Oxidative stress is involved in the development of pulmonary hypertension syndrome (PHS) in broilers. l-Carnitine has an antiperoxidative effect and supplemental l-carnitine has been revealed to increase broiler heart weight. The present study was conducted to evaluate the effect of an addition of 100 mg/kg l-carnitine to the basal diets on PHS mortality in cold-exposed broilers. Two-hundred and forty mixed-sex broilers were equally assigned to three groups. The control group was reared in normal temperatures throughout the experiment. Starting on day 14 continuing until the end of the experiment, the other two groups were subjected to a step-down temperature programme (by lowering the temperature 1-2 degrees C per day down to 12-14 degrees C) with or without l-carnitine added to the basal diets. Cold exposure increased the right/total ventricle ratio (RV/TV) and plasma malondialdehyde (MDA), reduced superoxide dismutase (SOD) and led to pulmonary vascular remodelling in birds without feeding additional l-carnitine. Supplemental l-carnitine reduced plasma MDA, increased SOD, inhibited remodelling and postponed the occurrence of PHS for 1 week in cold-exposed broilers; nevertheless, it did not significantly influence the cumulative PHS mortality (p > 0.05). On days 24 and 32, birds fed supplemental l-carnitine had lower RV/TV and higher total ventricle/body weight (p < 0.05) but unchanged right ventricle/body weight ratios (p > 0.05) compared to their cold-exposed counterparts, indicating an increase in left ventricle weight. However, from day 39 on, their RV/TV ratios were suddenly increased (p < 0.05). It was suggested that the l-carnitine-induced increase in left heart weight might partially account for the postponed occurrence of pulmonary hypertension in the early stage by elevating cardiac output, which might, in turn, lead to the resulting increase in pulmonary pressure. In view of its complex effects on cardiopulmonary haemodynamics, l-carnitine supplementation may be impractical for reducing PHS.     

Quantitation of intestinal D-xylose absorption in normal broilers and in broilers with pale-bird syndrome

A micromethod was used in order to quantitate intestinal D-xylose absorption in young and extremely small birds. This test was performed in broilers collected from two farms from which birds were extremely uneven in body size and were passing poorly digested or undigested feed. A similar syndrome had been seen on all grow-outs during the 6 months before this investigation. Broilers were also collected and tested from three farms where no clinical signs of disease were seen. D-Xylose absorption peaks and curves for normal broilers closely resembled those observed in normal humans. Mean plasma D-xylose concentrations for virus-infected broilers and for broilers with pale-bird syndrome were consistently lower than concentrations for normal broilers (P = 0.009). Reoviruses, small coronavirus-like particles, small round virus particles, and abundant bacterial flagellar fragments were seen in fecal samples from broilers with pale-bird syndrome. Production performance was lowest on farms showing clinical signs of this syndrome.     

Erythropoiesis regulation during the development of ascites syndrome in broiler chickens: a possible role of corticosterone

The ascites syndrome in broiler chickens is attributed to metabolic burdening, which results from intensive genetic selection for rapid growth coupled with exposure to extreme environmental conditions, such as low ambient temperature. These conditions impose on the broilers difficulties in fulfilling tissue demands for oxygen, and the birds exhibit a decrease in blood oxygen saturation and high hematocrit values. It is unknown whether the increase in hematocrit results from alteration in erythropoiesis or from fluid exudation out of the blood system to the abdominal cavity. The present study was conducted to examine the association between abnormal stress response and erythropoiesis process in ascitic broilers. Ascitic chickens revealed a uniquely continuous stress response: expressing an increase (P < or = 0.05) in plasma corticosterone concentration 2 to 3 wk before death. At 5 wk of age, ascitic broilers exhibited an increase (P < 0.05) in hematocrit, blood cell count, and packed cells and blood volumes, with no significant change in plasma volume. These results confirm an accelerated erythropoiesis process in ascitic birds. Increased blood cell production in ascitic birds was matched by an increase (P < 0.05) in the proportion of immature red blood cells (23%) in comparison with broilers that remained healthy (7%), and by decreased (P < 0.05) hemoglobin content relative to red blood cells. We conclude that continually increased corticosterone concentrations, as an inducer of erythropoiesis proliferation and differentiation arrest, in ascitic chickens, resulted in increased production of red blood cells (partially immature) with decreased hemoglobin content; this decrease in hemoglobin might have contributed to enhanced development of hypoxemia and to aggravation of the syndrome.     

Effect of pelleted feed on the incidence of ascites in broilers reared at low altitudes

A study was conducted to investigate whether the use of pelleted feeds might influence the incidence of ascites in broilers reared at low altitudes (730 meters above sea level). In two trials carried out under commercial conditions, broilers were fed practical-type rations from 1 day to 7 weeks of age, in either mash or pellet form. In both trials, low incidences of ascites (less than 5%) were recorded for broilers receiving feed as pellets. No cases of the syndrome were observed in birds fed mash, either in the field or at the processing plant. These data suggest that the positive relationship between pelleted feeds and incidence of ascites observed at high altitudes also exists at lower elevations.     

肉鸡腹水症发病机理研究Ⅳ.肉鸡和蛋仔鸡左右心室功能的比较研究

试验选用快速生长的艾维茵肉鸡和海兰蛋仔鸡 ,各试验组用右心导管法和左心导管法测定肺动脉压(PAP)、右心室收缩压 (RVSP)、左心室收缩压 (LVSP)、左右心室内压最大变化速率 (+dp/dt)的动态变化。并且比较了相同体重健康蛋仔鸡、肉鸡的左右心室功能变化特点。结果表明 :相同日龄肉鸡肺动脉压显著高于蛋仔鸡 ;2 8、35日龄肉鸡右心收缩压显著高于蛋仔鸡 (P <0 0 5) ,2 8、35、42和 49日龄肉鸡左心室收缩压低于蛋仔鸡 ,且差异极显著 (P <0 0 1 )。肉鸡左心室内压最大变化速率 (LV +dp/dt)从 2 1日龄测定起呈现显著性低于同日龄的蛋仔鸡。相同体重的肉鸡和蛋鸡相比 ,肉鸡肺动脉压 (PAP)显著高于蛋仔鸡 ,但肉鸡右心室内压最大变化速率 (RV +dp/dt)、左心室收缩压 (LVSP)、左心室内压最大变化速率 (LV +dp/dt)显著低于蛋仔鸡。这提示肉鸡先天存在着肺动脉压较高、左心室病理性功能低下 ,这可能是肉鸡容易发生腹水症的原因之一     

Activation of PKCalpha and pulmonary vascular remodelling in broilers

OBJECTIVE: The present study was conducted to examine the presence of protein kinase Calpha (PKCalpha) in the pulmonary arterioles of broilers during the development of pulmonary hypertension and pulmonary vascular remodelling. METHOD: One hundred and sixty day-old Avian-2000 broilers were divided equally into a control group and a cold temperature group. All the birds were reared in normal temperatures up to day 14, with the lighting schedule at 24 h per day. Thereafter, birds in the cold temperature group were subjected to low temperature by lowering 1-2 degrees C per day to 12-14 degrees C, and then kept constant until day 49, while birds in the control group were still brooded at normal temperatures. All the birds were fed a diet of pellets throughout the study. Samples of blood were taken from the wing vein, and of heart and lung collected after the birds were killed with an overdose of sodium pentobarbitial, at days 24, 32, 39 and 45 of age, respectively. Right ventricle to total ventricle ratio (RV/TV) and packed cell volume (PCV) were measured. Vessel wall area to vessel total area ratio (WA/TA) and mean media thickness in pulmonary arterioles (mMTPA) was examined using computer-image analytic software. Expression of PKC in pulmonary muscular arterioles was assessed by immunohistochemistry and quantified by measuring optical density (OD) using computer-image analytic software. RESULTS: The incidence of pulmonary hypertension syndrome (PHS) was 12.5% in birds exposed to cold, and 3.75% in the control group (P<0.05). PCV in the cold temperature group was elevated after day 32 (P<0.05), and RV/TV ratio increased on day 45 (P<0.05). Both the WA/TA and mMTPA of birds subjected to cold were significantly elevated (P<0.05). The OD values were not significantly increased before day 32 (P>0.05), however, one week later (at day 39 of age), the difference between the two groups was significant (P<0.05). The increased PKCalpha expression was positively correlated with the values of mMTPA and WA/TA. CONCLUSION: PKCalpha expression was up-regulated during the development of pulmonary hypertension. The activation of PKCalpha might be involved in the development of pulmonary vascular remodelling.     

In vitro and in vivo characterization of avian reoviruses. I. Pathogenicity and antigenic relatedness of several avian reovirus isolates

Pathogenicity, pathogenesis, and antigenic relatedness of four avian reovirus isolates obtained from commercially reared broilers were investigated. Chickens of various ages were inoculated both orally and intratracheally with reovirus. Based on disease signs, mortality, weight depression, tissue lesions, invasiveness, and viral persistence in chickens inoculated at 1 day of age, the isolates were classified as being of low, intermediate, or high pathogenicity. The low-pathogenicity isolate (2177) did not cause mortality, weight depression, or clinical disease. The isolate of intermediate pathogenicity (2035) produced low mortality rates (8%), some weight reduction by 7 weeks postinoculation, and microscopic lesions in the intestine and gastrocnemius tendons. The pathogenic isolates, 2408 and 1733, caused severe clinical disease characterized by stunting, feathering abnormalities, mortality as high as 84%, and microscopic lesions in the liver, intestine, pancreas, and/or gastrocnemius tendon. Highly pathogenic isolates also persisted longer in tissues of infected birds and elicited a more prompt and prolonged antibody response. Birds inoculated at 1 day or 1 week of age were more susceptible to reovirus-induced disease than birds inoculated at 2 weeks, suggesting an age-associated resistance. All isolates produced mortality with equal frequency in embryos. The isolates characterized were found to be antigenically similar based on cross-neutralization and cross-protection studies.     

Cellular immune response in the small intestine of two broiler chicken lines orally inoculated with malabsorption syndrome homogenates

We studied the cellular immune response against malabsorption syndrome (MAS) in two broiler chicken lines, A and B. We determined the number of pan T-lymphocytes (CD3), helper T-lymphocytes (CD4), cytotoxic T-lymphocytes (CD8) and macrophages/monocytes in the small intestine in the first 2 weeks after oral inoculation of two MAS homogenates, MAS80 and MAS97-1. The immune cells were detected on cryostat tissue by immunohistochemistry and counted by villus area. In trial 1, we compared the two broiler lines for weight gain depression, intestinal lesion and number of CD3, CD4, CD8 cells and macrophages/monocytes after MAS80 inoculation. Although there was no significant difference in weight gain depression between the two broiler lines, line B had significantly higher numbers of CD8+ T-cells per villus area than had line A. To confirm part of the results of trial 1, trial 2 was done in which we compared different homogenates in broiler line B. Broiler line B was orally inoculated with either MAS97-1, intestinal homogenate obtained from healthy chickens (healthy homogenate), or phosphate buffered saline (PBS). In this trial, the MAS97-1 homogenate also induced weight gain depression and intestinal lesions, whereas the "healthy homogenate" and PBS did not induce weight gain depression or intestinal lesions. The broilers inoculated with MAS97-1 homogenate had significantly more CD8+ T-cells per villus area than had broilers inoculated with "healthy homogenate" or PBS. Increased CD8+ T-cells per villus area in the affected small intestines of broilers suggests an increase of cytotoxic T-cell activity.     

A comparative study of the pathogenesis of malabsorption syndrome in broilers

Five malabsorption syndrome (MAS) homogenates from The Netherlands and Germany were used to reproduce MAS in broilers. We studied the histopathology after inoculation of 1-day-old broiler chicks and the agents that might be involved. Generally, the MAS homogenates induced signs that differed in severity and pathobiology. We could distinguish and classify the inoculated groups best by histopathology: proventriculitis, lesions in the small intestines in combination with proventriculitis, or lesions of the small intestines only. Lesions in the small intestine had more impact on weight gain depression than lesions in the proventriculus. In three out of five inoculated groups, microscopic lesions of the pancreas were found. Reovirus was detected in the inoculated groups by virus isolation and seroconversion, and reoviral antigen was detected by immunohistochemistry of the small intestine. Also, enteroviruslike particles were detected in three of the five inoculated groups, although not in the most affected group. Additionally, bacteriophages and bacteria (hemolytic Escherichia coli, Pasteurella hemolytica, and Enterococcus durans) were isolated from inoculated chicks. The role these agents play in pathogenesis of MAS is still unsolved.     

Presence of inoculated Campylobacter and Salmonella in unabsorbed yolks of male breeders raised as broilers

Day-old male broiler breeder chicks were obtained from a commercial hatchery and raised as broilers. For Experiment 1, at 5 wk of age, the broilers were orally inoculated with a 10(6) cfu/ml of a characterized strain of Campylobacter jejuni and a cocktail (three naladixic acid-resistant strains) of Salmonella serovars. One week after inoculation, the birds were euthanatized and defeathered. The abdominal cavity was examined and any unabsorbed yolk material (and remaining yolk stalk) and ceca were aseptically removed for microbiological analyses. For each pooled sample (two birds per pool), an aerobic plate count (APC), an Enterobacteriaceae (ENT) count, and a test for the presence of Campylobacter and Salmonella was performed. For Experiment 2, at 5 wk of age, the broilers were orally inoculated with 10(5) cfu/ml of a characterized strain of Campylobacter jejuni. One week after inoculation, the birds (n = 20) were killed, defeathered, and the yolk stalk, attached yolk, or free-floating yolk and ceca were individually analyzed for presence of Campylobacter. For Experiment 1, the Salmonella-inoculated birds had 2/12 ceca and 0/12 unabsorbed yolk samples positive for Salmonella. The average yolk APC was log10 3.4 cfu/g and the average ENT was log10 1.9 cfu/g. For the Campylobacter-inoculated birds, 12/12 ceca and 9/12 unabsorbed yolk samples were positive for Campylobacter. The average yolk APC was log10 3.5 cfu/g and the average ENT was log10 3.1 cfu/g. For Experiment 2, the inoculated Campylobacter birds had 19/20 ceca, 5/20 free floating yolks, and 19/20 yolk stalks positive. In Experiment 1, the inoculated Campylobacter colonized the ceca in every instance and were present in 75% of the unabsorbed yolks. Alternatively, the inoculated Salmonella were not found in any of the unabsorbed yolks and only rarely in the ceca. In Experiment 2, the inoculated Campylobacter was found in very high numbers in the yolk and internal body samples. Determining to what extent these internal bodies and unabsorbed yolks play in bacterial colonization and contamination of the birds at processing has not been determined. The next step will be to determine the incidence of unabsorbed yolks and presence of Campylobacter and Salmonella in these bodies of commercial broilers at processing.     

Progressive bradycardia,a possible factor in the pathogenesis of ascites in fast growing broiler chickens raised at low altitude

1. The first objective was to evaluate baseline heart rate (HR) responses in fast growing broilers fed ad libitum from 1 to 45d or subjected to a food restriction (85%, 70% and 55% of ad libitum from 7 to 21d) and a refeeding (22 to 45d) regimen in a normal thermal environment. The second was to evaluate HR and haematocrit responses in fast growing broilers reared at a low environmental temperature and fed ad libitum (A-L) from 1 to 42d, subjected to food restriction (70% ad libitum ) between 7 to 21d and refed thereafter (R-R), or subjected to food restriction between 7 to 42d (R), and to follow the changes in normal birds and those prone to ascites. 2. The baseline HR in the normal thermal environment at 21 and 45d in birds fed ad libitum was lower (P < 0.001) than at 7d. The food-restricted groups had higher HRs at 21d than at 7d, with the differences significant (P < 0.01) for the 70% and 55% treatments. At 21d the HRs in restricted groups were significantly higher (P < 0.01) than in ad libitum -fed birds. After returning to ad libitum feeding the HRs in these birds tended to decline, with the differences significant (P < 0.05) for the 70% and 55% treatments. 3. In the birds exposed to cold, each feeding regimen produced distinct patterns of change in HR and haematocrit. Both feeding regimen and age had significant (P < 0.001) effects on the changes of both variables. Relative to 7d, on 14d and 21d the HRs decreased and haematocrits increased in all groups, but the rates of change were highest in the A-L and R-R birds. The first fulminant cases of ascites were observed during the third week in the A-L group and during the fourth week in the R-R group. None of the chickens from the R group developed ascites. Altogether, the incidence of ascites was 48% in the A-L group and 28% in the R-R group. 4. Among the birds exposed to cold, the ascitic birds had significantly (P < 0.001) lower HRs and higher haematocrits than normal birds from the same feeding regimen group. The time trends in the rates of change in HR and haematocrit were distinctly different (P < 0.001) for ascitic and normal birds. The change in feeding regimen from restricted to ad libitum in the R-R group resulted in a significant (P < 0.001) decrease in HR and increase in haematocrit. 5. In view of the evidence presented, it appears that hypoxaemia and tissue hypoxia in broiler chickens may be a result of circulatory insufficiency associated with progressive bradycardia rather than, as commonly believed, pulmonary insufficiency. In this situation the pulmonary hypertension may be a secondary symptom.     

Oocyst output and transmission rates during successive infections with Eimeria acervulina in experimental broiler flocks

The infection dynamics of Eimeria species determine the clinical manifestation of the disease coccidiosis in poultry flocks, and a better understanding of the dynamics may contribute to improvement of control measures. Our aim was to study the course of infection and the transmission of Eimeria acervulina in groups of broilers by quantifying the transmission rate parameter and oocyst output. Three transmission experiments were carried out with groups of 20 male SPF broilers. At 2 days of age, one bird in each trial was orally inoculated with five sporulated E. acervulina oocysts (D0 post-inoculation, pi). One day after inoculation (D1 pi), the inoculated bird was housed with 19 non-inoculated contact birds. Individual faecal droppings were examined daily from D3-D32 pi to quantify the number of oocysts per gram faeces. The inoculated bird started shedding oocysts at D5 pi and contact birds between D10 and D17 pi. Contact birds that became infected due to oocyst excretion by the inoculated bird were characterized as first generation contact birds (C1). Contact birds excreting from D15 pi onwards (C2) became infected after the first C1 birds had started shedding and were considered to belong to a successive generation of the flock infection. Oocyst output was significantly lower for C1 compared to C2 birds, but the transmission rate parameter remained constant for both infection generations. These results suggest that although oocyst load increases, the transmission rate of E. acervulina remains constant between successive generations of infection in a flock.     

Ubiquitin gene expression and ubiquitin conjugation in chicken muscle do not reflect differences in growth rate between broiler and layer birds.

Previous work has shown that chicken strains selected for growth (broilers) degrade muscle proteins less rapidly than those selected for egg laying. They also have decreased calpain and increased calpastatin content in breast muscle. This study aimed to test the hypothesis that these differences correlate with changes in the ATP- and ubiquitin-dependent proteolytic system. Chickens of a broiler strain (Ross 1) and a layer strain (ISABrown) were reared to the age of 4 wk under identical conditions with ad libitum access to feed and water. Mean fractional growth rates were 10.4%/d for broilers and 7.4%/d for layers. Feed intake measured in the last week of the trial was slightly greater in layer birds (.11 and .12 g x g body weight(-1) x d(-1) for broilers and layers respectively; P < .006). Polyubiquitin (UbI) messenger RNA was abundant in the muscles of these well-fed birds, but it showed little difference between strains. Muscle did not significantly express the UbII polyubiquitin gene. The ATP-dependent system conjugating ubiquitin to endogenous proteins had greatest activity in the gastrocnemius muscle of broiler birds but was not significantly different between breeds. Proteins cross-reactive with antisera to recombinant human proteasome regulatory subunits MSS1 (multicopy suppressor of SUG 1; S7) and TBP1 (tat binding protein 1; S6') were present in muscle homogenates from both strains of bird. The chick equivalent of TBP1 was more abundant in breast muscle of broiler birds than in leg muscle, or in either muscle of layers. Antiserum to recombinant yeast subunit mts2 (mitosis temperature sensitive gene 2; S4) did not react with any protein of the expected size but detected a 30-kDa peptide that was not associated with the 26S proteasome; this was found only in muscle from the layer strain. Hence, during normal growth of chickens, rates of protein degradation are not controlled by the expression of ubiquitin mRNA or the conjugation of ubiquitin. However, the composition of the 26S proteasome may be a regulatory factor.