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Ana Jurnal 1 PDF
Ana Jurnal 1 PDF
DESCRIPTION OF PROBLEM
Ascites in broilers is associated with factors such as fast growth rate and environmental pa- rameters, including
low ambient temperatures
1 Corresponding author: sezen.ozkan@ege.edu.tr
(T
a
) and high altitude [1]. The syndrome is de- fined as a circuit of events between the cardio- vascular and
pulmonary systems responsible for metabolic demands [2]. The association of asci- tes with cardiopulmonary
capacity and its ge-
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JAPR: 10 Research Report netic background have been clearly demon- strated [3, 4], and Decuypere et al. [5]
concluded that the hypothyroid state associated with the decreased metabolism for maintenance that is caused by
continuous selection for fast growth and improved feed efficiency might be involved in ascites. The high metabolic
rate in fast-grow- ing chickens, which increases dramatically in response to environmental conditions, leads to the
development of the ascites syndrome, which may be characterized by enhancement of the erythropoiesis process [6].
This enhancement leads to a dramatic increase in the number of immature erythrocytes in the circulation and to a
decline in the heart rate during early periods of growth [7]. These events lead to the develop- ment of hypoxemia
[1], which can be confronted effectively by reducing oxygen demands, a mea- sure that can be achieved by early-age
feed re- striction.
Early growth restriction induced by feed re- striction has resulted in improved feed effi- ciency, because of the
decrease in energy re- quirements for maintenance, and improved car- cass quality resulted from the decline in fat
deposition [8, 9]. Despite this, conflicting find- ings have resulted from variations in the duration and severity of the
restriction, but, nevertheless, restriction of feed either as nutritional quality or quantity of feed or time accessing to
feeders is one of the primary management tools currently used to reduce the incidence of ascites in broiler
production [1, 10, 11, 12, 13, 14, 15, 16]. Feed restriction mainly reduces growth rate and, con- sequently, metabolic
demands, during the criti- cal periods of the life span of a bird [11, 12, 13, 14, 15, 16, 17, 18], and it is associated
with improvement in arterial oxygenation [10]. How- ever, feed restriction can exert negative effects on the body
weight at marketing age [13] and on the relative weight of breast muscle [12]. There have also been reports of
negative effects on thyroid gland activity [19] and on the plasma triiodothyronine (T
3
(FCR) [23]. Recently, Luger et al. [24] reported that chickens that developed ascites could not produce T
4
at a sufficient rate to compensate for the reduction caused by exposure to cold, which coincided with
reduced T
3
concentrations. A possible role of thyroid hormones in the develop- ment of the ascites
syndrome has been sug- gested [6].
The objective of the present study was to elucidate the role of early-age food restriction on the development of
the ascites syndrome and performance related parameters in broilers reared under cold conditions from 3 wk of age
onward.
MATERIALS AND METHODS
Experimental Design
Male broiler chicks (Cobb) were obtained from a commercial hatchery and housed in bat- tery brooders under
standard management con- ditions for the first 5 d of age. At 5 d, 76 chicks were weighed, wing-banded, and
randomly di- vided between 2 feeding groups with 7 replicates of 5 to 6 birds each. The chicks were exposed to T
a
of 26.0 ± 1.0, 20.0 ± 1.0, and 15.0 ± 1.0°C at 7, 18, and 21 d of ages, respectively, to induce the development
of ascites syndrome. At the age of 21 d, the birds were transferred to colony cages in a temperature-controlled room
and kept at 15°C and 60% relative humidity until 46 d of age.
Feeding
Control birds were fed ad libitum (AL) dur- ing the experiment. In the growth-restricted group, chicks were
exposed to feed restriction (FR) from 5 to 11 d of age; each chick was allowed a daily intake 18.7 g of feed that con-
tained sufficient energy to support 50% of the normal growth rate. The energy allowance dur- ing FR was calculated
according to the following equation modified from Plavnik and Hurwitz [9, 25]:
EA = M × BW0.667 + G × GA
where EA = energy allowance (kcal), M = main- tenance requirement (1.5 kcal/g), BW0.667 = met- abolic body
weight at the beginning of the feed restriction period (5 d), G = energy requirement
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) concentration [20]. Alteration in thyroid hormone metabolism in ascites-susceptible broilers has
been cited by several authors [21, 22, 23, 24], and low plasma triiodothyronine (T
4
) concentration at low T
a
has been reported to indicate thyroid insufficiency associated with
ascites incidences in lines with a fast growth rate and low feed conversion ratio
̈ O
ZKAN ET AL.: EARLY FEED RESTRICTION AND ASCITES DEVELOPMENT 11
for 1 g of growth (2 kcal/g), and GA = growth allowance (15 g/d).
A crumble form of starter diet was supplied from d 0 to 21, and a pelleted grower diet was supplied from d 21 to
46 of the experiment. The diets were designed according to the National Research Council’s recommendations [26]
and contained 3,100 and 3,200 kcal/kg of metabolic energy, respectively, and 22.6 and 19.6% of crude protein,
respectively. Water was available AL, and continuous fluorescent illumination was applied to the broilers during the
experimental period.
Individual body weights were measured at 5, 11, 18, 25, and 46 d of age. Feed consumption was recorded
weekly, and FCR were determined for each replicate (cage) based on feed consump- tion and body weight gain
including birds that died during the entire period.
Blood samples were taken on d 30 and 37 from the brachial vein. The blood samples were stored at 4°C for
hematocrit analyses, and an aliquot was centrifuged at 3,000 rpm for 10 min to obtain plasma, which was stored at
−20°C pending further analyses.
Ascites Diagnosis
During the experiment, all dead chickens were diagnosed for ascites according to abdomi- nal and pericardial
fluid accumulation and right heart enlargement. At the end of the experi- ments, all chickens were euthanized to
detect ascites according to fluid accumulation in the body cavities and to right heart enlargement [right ventricle
weight per total ventricle weight (RV:TV) ratio > 0.28]. The birds that showed these symptoms were considered
ascitic and were included in the analysis of all parameters regarding ascites. Birds not showing any of these
symptoms were classified as healthy in all statis- tic analysis of each age. Birds having a slight hydropericardium but
not showing right heart enlargement were also classified as healthy.
Breast muscle (pectoralis major and minor), abdominal fat pad, lung, heart, liver, and spleen were dissected and
weighed. The RV:TV ratios were calculated.
Hematocrit
Blood in heparinized microcapillary tubes was centrifuged for 7 min for hematocrit (HCT) measurements.
Thyroid Hormones
Plasma samples were radioimmunoassayed for total T
4
and T
3
with commercial kits [27] validated for domestic fowl [28]. The T
3
assay was characterized by intraassay and interassay CV of 7.0 and 9.4%,
respectively, and the T
4 assay by intraassay and interassay CV of 5.0 and 7.5%,
respectively. The T
3
assay was carried out according to the manufacturer’s instructions without
modifications, whereas in the T
4
analy- sis 100-μL samples were used.
Oxygen Consumption
On 3 consecutive days during the sixth week of age the oxygen consumption of 14 (7 from each feeding group)
broilers was measured with an oxygen analyzer [29] according to the proce- dures of Yahav and Buffenstein [30].
Birds were chosen for measurement according to their pre- viously measured HCT levels. For this purpose, 3 or 4
birds with high (>41%) or low (<41%) HCT were chosen from each feeding group, but the final descriptions of the
birds as either ascitic or healthy were confirmed by necropsy at slaughter or death.
Statistical Analysis
Data, except for feed consumption and FCR, were subjected weekly to 2-way ANOVA with respect to the
following main effects: ascites (ascitic or healthy birds), feeding (FR or AL feeding), and their interaction using the
JMP statistics software package [31]. Body weight on d 5 was included in the model as a covariance parameter for
the body weight and weight gain data. Only feeding effect was included in the statistical model for feed
consumption and FCR data. Least square means were separated with Student’s t-test [32]. The distribution of ascites
incidence and mortality within feeding groups were analyzed with the chi-squared test. Shapiro Wilk’s normality
test was performed on all data and, if necessary, a common log transformation was applied to the T
3
, T
4
, and HCT data to obtain a normal distribution [32]. Actual values, however, are
presented in the tables.
RESULTS Ascites Incidence and Mortality
The feed restriction treatment reduced the total mortality, mortality from ascites, and over-
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JAPR: 12 Research Report Table 1. Distribution of total mortality, mortality from ascites, ascites defined at slaughter, and total
ascites incidence within feeding groups
Total Mortality from Ascites defined Total ascites mortality ascites at slaughter incidence Trait (%) (%) (%) (%)
Feed restriction (FR) 18.42 7.89 7.89 15.79
n = 7/38 n = 3/38 n = 3/38 n = 6/38 Ad libitum (AL) 39.47 26.32 10.53 36.84
n = 15/38 n = 10/38 n = 4/38 n = 14/38 Overall (FR + AL) 28.94 17.10 9.21 26.32
n = 22/76 n = 13/76 n = 7/76 n = 20/76 χ2 = 4.166* χ2 = 4.756* χ2 = 0.158 χ2 = 4.438*
*P < 0.05.
all ascites incidence (Table 1) significantly (P < 0.05). Ascites mortality was first observed 1 wk after cold exposure,
and all mortality oc- curred during the fifth (6 birds) and sixth (7 birds) weeks (data not shown).
Body Weight and Gain
Feed restriction resulted in a lower body weight (P < 0.05; Table 2). However, at the end of the experiment, FR
broilers achieved body weights similar to those of the AL birds. During the feed restriction period (d 5 to 11), the FR
group gained 38.94% of the weight that the AL gained. During the first week posttreatment (d 11 to 18) the FR
broilers gained significantly more weight than the AL ones (P < 0.05), which suggests that their growth accelerated
during this stage of life. On the other hand, the FR birds did not show any further compensatory growth even during
the later stages of life. There was no interaction between ascites and feeding regi- men for body weight and weight
gain at any age (Table 2). The body weights of ascitic and healthy birds differed significantly only at the age of 46 d
(P < 0.05).
Feed Consumption and FCR
The cumulative feed consumption and FCR (5 to 46 d) did not differ between the feeding regimens (Table 3).
The FR group performed better than the AL group from d 11 to 25 (P < 0.05).
Relative Weights of Organs
Ascites affected all carcass parameters with the exception of the abdominal fat (Table 4).
At slaughter age, ascitic broilers had smaller relative weights of breast muscle and spleen than those of the healthy
birds, but the relative weights of lung, heart, and liver and RV:TV ratios were greater in the ascitic ones (P < 0.05).
The feeding regimen did not affect any of these above parameters (Table 4). No interactions among the treatments
were observed in their effects on any of these traits.
Hematocrit
A significant effect of ascites on HCT was observed at 37 d of age (P < 0.05; Table 5). Ascitic birds had
significantly higher hematocrit values than the healthy birds. However, the feed- ing regimen did not affect the HCT
measure- ments at 30 and 37 d.
T
3
and T
4
Hormones
The plasma T
3
concentration was signifi- cantly lower in ascitic than in healthy broilers at 30 and 37 d of age
(P < 0.05) but was not affected by FR at these ages (Table 5).
The plasma T
4
concentration was lower in ascitic than in healthy birds only at 37 d of age, whereas FR birds
exhibited a significantly higher plasma T
4
concentrations than the AL birds at 30 d (P < 0.05; Table 5). The interaction of ascites × feeding regimen
was not significant for either trait at any age. However, at 30 d of age in the FR group, T
3
levels of ascitic broilers were similar to those of healthy birds (2.51 and 2.62 ng/mL,
respectively), whereas in the AL group T
3
levels differed significantly (P < 0.05) between ascitic and healthy broilers (1.92 and 2.99 ng/mL,
respectively; data not shown).
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ZKAN ET AL.: EARLY FEED RESTRICTION AND ASCITES DEVELOPMENT 13
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JAPR: 14
Research Report Oxygen Consumption
Oxygen consumption was lower in ascitic than in healthy birds (P < 0.05; Table 6). Feeding did not affect
oxygen consumption and the asci- tes × feeding interaction was not significant.
DISCUSSION
The results obtained emphasize the signifi- cant and positive effects of feed restriction in preventing the
development of the ascites syn- drome in broiler chickens.
Performance and Mortality
Feed restriction from 5 to 11 d of age reduced weight gain (to 38.9% of that in the AL broilers) and reduced FCR
during the restriction period. Following the restriction period (11 to 18 d of age), compensatory growth was
observed in the FR birds. It seems that the severity of the restric- tion period allowed full growth compensation up to
the marketing age, as was previously reported [8, 9, 11, 17, 20, 22, 33, 34, 35]. The FR resulted in a marked
reduction of ascites incidence and mortality compared with AL feeding, which is consistent with previous findings
[11, 18, 13, 14]. In general, susceptibility to ascites has been asso- ciated with high growth rates [1, 36], and a posi-
tive correlation between potential growth rate and percentage ascites has been reported by Deeb et al. [37]. In the
present study, the retardation of growth rate during the FR period could have been the main reason for the decline in
ascites inci- dences and mortality, but it should be noted that other studies have found that ascitic broilers are not
necessarily the fastest growing individuals in the flock [4, 24, 38, 39]. Furthermore, detrimental effects of ascites on
body weight have been re- ported previously [1, 38], and those findings are consistent with the lower body weights
of ascitic broilers at marketing age that was found in the present study. Acceleration of growth in FR broiler
accompanied with low ambient tempera- ture could result in hypoxemia and trigger the ascites. However, this was
not the case and FR resulted in late maturity and lower incidence of ascites in this experiment, which that FR might
affect the development of ascites in a critical stage prior to low T
a
exposure. In general, the present findings on the relative weights of carcass parts and internal organs and
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ZKAN ET AL.: EARLY FEED RESTRICTION AND ASCITES DEVELOPMENT 15
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JAPR: 16 Research Report Table 5. Effect of ascites and feeding regimen on hematocrit (HCT), triiodothyronine (T
3
), and thyroxine (T
4
) levels of broilers at 30
and 37 d of age
HCT (%) T
3
(ng/mL) T
4
(ng/mL)
d 30 d 37 d 30 d 37 d 30 d 37
Ascites1
Ascitic 36.95 ± 1.03 40.24 ± 1.31a 2.21 ± 0.20b 1.94 ± 0.26b 3.29 ± 0.33 1.43 ± 0.32b
(n = 18) (n = 13) (n = 12) (n = 10) (n = 12) (n = 10) Healthy 36.19 ± 0.59 36.59 ± 0.67b 2.80 ± 0.16a 2.73
± 0.19a 3.03 ± 0.26 2.48 ± 0.23a
(n = 40) (n = 48) (n = 18) (n = 19) (n = 18) (n = 19) Feeding
FR2 35.89 ± 0.91 37.64 ± 1.12 2.56 ± 0.19 2.56 ± 0.23 3.78 ± 0.33a 2.12 ± 0.28
(n = 32) (n = 33) (n = 13) (n = 15) (n = 13) (n = 15) AL 37.25 ± 0.76 39.19 ± 0.96 2.45 ± 0.16 2.11 ± 0.23
2.54 ± 0.26b 1.79 ± 0.28
(n = 26) (n = 28) (n = 17) (n = 14) (n = 17) (n = 14) P-values Source of variation
Ascites 0.524 0.024 0.028 0.021 0.546 0.014 Feeding 0.256 0.364 0.650 0.171 0.007 0.415 Ascites × feeding 0.150 0.256 0.069
0.375 0.224 0.289
a,bValues with different superscripts for each main effect within age (column) differ (P < 0.05). 1Classification of birds as ascitic
or healthy; ascitic data were derived from dead birds plus those inspected at the end of the experiment and having fluid
accumulation in the abdomen, pericardium, or both and right heart enlargement (right ventricle weight per total ventricle weight
> 0.28). 2FR = feed restriction; AL = ad libitum.
on the RV:TV ratios of ascitic broilers are consis- tent with previous results [1, 4, 5]. Increased RV:TV ratios and
relative weights of heart, lung, and liver reflected the enlargement of the right side of the heart and edema in the
supply organs.
Table 6. The effects of ascites and feeding regimen on oxygen consumption of broilers at the age of 6 wk
Oxygen consumption Ascites1 (mL/g per h; STP)2
Ascitic 2.22 ± 0.43b Healthy 3.29 ± 0.37a Feeding3
FR 3.00 ± 0.40 AL 2.51 ± 0.40 Source of variation P-values Ascites 0.043 Feeding 0.319
a,bValues with different superscripts for each main effect within age (column) differ (P < 0.05). 1Classification of birds as ascitic
or healthy; ascitic data were derived from dead birds plus those inspected at the end of the experiment and having fluid
accumulation in the abdomen, pericardium, or both and right heart enlargement (right ventricle weight per total ventricle weight
> 0.28). 2STP = standard temperature and pressure. 3FR = feed restriction; AL = ad libitum.
The significantly lower relative weight of the spleen of ascitic broilers could be attributed to the stress responses of
the birds. In general, re- gression of lymphoid organs (e.g., the spleen) is recognized as an important response of
chickens to chronic stress [40, 41]. Significant reduction in abdominal fat pad size [8, 9, 34] and greater heart weight
as a percentage of body weight [14, 20] in growth-restricted birds have been reported before, but these traits were
not affected by feed- ing in the present study.
The present findings showed that better FCR in FR than in AL broilers coincided with greater weight gain
between 11 and 18 d of age, but the FR birds did not perform better than the AL ones over the whole production
period. This finding is contrary to those of previous studies, which reported improvements in overall feed
conversion ratio as the most consistent result of early feed restriction studies [8, 9, 13, 25, 33, 35, 42]. This
difference may be attributed to the pronounced effect of cold stress on FR birds. Increased heat production rate with
decreased ambient tempera- ture has been shown in broilers [43]. In the present study the FR birds were smaller by
the age of 46 d, probably because they had used a higher
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̈ O
ZKAN ET AL.: EARLY FEED RESTRICTION AND ASCITES DEVELOPMENT 17
proportion of energy for maintenance than for growth.
HCT, Thyroid Hormones, and Oxygen Consumption
Ascites had a significant effect on HCT levels at 37 d of age, and an increased HCT level is one of the defining
characteristics of the ascitic broiler [15, 24, 44, 45].
The lowest levels of T
3
to hypoxemia under cold and low oxygen pressure conditions (high altitude) have been suggested [1, 7, 15, 22, 46].
Our findings were consistent to the earlier study of Scheele at al. [47], who sug- gested that low oxygen
consumption per meta- bolic body weight at low T
a
indicated inadequate metabolic action and could lead to pulmonary hypertension syndrome (PHS) and, finally, asci-
tes in broilers. It coincided with higher HCT levels in a male line selected for improved FCR and growth rate as
compared with a standard broiler stock. In a recent study, Malan et al. [48] con- firmed the association between
ascites incidence and low heat production, thus oxygen consump- tion, per metabolic body weight. In the present
study the reduction in oxygen consumption could have been related to the development of the syn- drome, which
impaired the overall performance of the broilers (i.e., feed intake and weight gain). It can be concluded that FR
significantly re- duced the development of ascites, as it can be induced by other methods (e.g., light restriction,
dietary energy, or using mash vs. pellet diets) [11, 16, 49, 50, 51]. The FR induced better FCR in FR broilers, which
consequently exhibited greater weight gain from d 11 to 18. However, the FR broilers did not retain this advantage
over the AL birds for the whole of the production period, possibly because of the more pronounced effect of cold
stress on the FR birds than on the AL ones in the present study. The lower oxygen con- sumption observed in the
ascitic birds during their sixth week of age could be attributed to the overall deterioration of the birds’ conditions.
However, further research is required to elucidate this question.
3. Wideman, R. F., Jr., Y. K. Kirby, R. L. Owen, and H. French. 1997. Chronic unilateral occlusion of an extrapulmonary
primary bron- chus induces pulmonary hypertension syndrome (ascites) in male and female broilers. Poult. Sci. 76:400–404.
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and T
4
hormones that were observed at the ages of 30 and 37 d in the present study are in
accordance with the results of Luger et al. [24], who reported lower plasma T
3
and T
4
concentrations in ascitic broilers than in healthy birds approximately 1 wk before the death of the former.
Plasma T
4
concentrations in the FR broilers were higher than those in the AL birds at d 30, and
increased thyroid hormone activities during the compensatory growth period was to be expected [13, 19].
The similarity of the T
3
levels in the ascitic and healthy FR broilers at 30 d of age (2.51 and 2.62 ng/mL,
respectively; data not shown) may lead to the conclusion that FR birds were able to keep plasma levels of T
3
high until they developed ascites. This, in turn, may indicate that growth restriction resulted in enhanced recovery of
thy- roid gland functions. However, even if this recov- ery was better, it was not to a high enough level to prevent
ascites development in all the FR broilers. The significantly lower oxygen consumption in the ascitic broilers was
measured at the age of 6 wk, when the syndrome was already developing, as was to be expected under cold
conditions that result in additional demands on the metabolic load on the birds. Increased incidence of ascites due
CONCLUSIONS AND APPLICATIONS 1. The FR significantly reduced the development of ascites and could be
used effectively as a
management treatment to prevent the development of the syndrome. 2. The FR used from d 5 to 11 enabled the
broilers to compensate for weight gain deficiency during
the treatment and to reach the same BW as the AL birds by marketing age (d 46). 3. Terminal stages of ascites
syndrome could be characterized by low oxygen consumption.
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