| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
|
|
|
|||||||
|
|||||||||
GENETICS |
* Faculty of Agricultural, Food and Environmental Quality Sciences, Hebrew University of Jerusalem, Rehovot 76100, Israel; and Kimron Veterinary Institute, Bet Dagan 50250, Israel
1 Corresponding author: cahaner{at}agri.huji.ac.il
 |
ABSTRACT |
|---|
 TOP ABSTRACT INTRODUCTIONMATERIALS AND METHODSRESULTSDISCUSSIONREFERENCES |
|---|
Key Words: ascites • broiler • early growth rate • oxygen saturation • heart rate
|
INTRODUCTION |
|---|
|
TOPABSTRACTINTRODUCTIONMATERIALS AND METHODSRESULTSDISCUSSIONREFERENCES |
|---|
The general pathogenesis of AS has been well documented (Maxwell et al., 1992; Julian, 1993; Shlosberg et al., 1998; Currie, 1999; Wideman, 2001, Balog, 2003). It is characterized by a cascade of events that begins with a lack of O2 for metabolism (Julian, 2000). The insufficient supply of O2 stimulates cardiac output, inducing increased vascular pressure in the lungs and pulmonary arteries. The pulmonary hypertension leads to a higher pressure load on the right ventricular muscle wall. This can lead to right ventricle hypertrophy and valvular in-sufficiency, causing a drop in cardiac output (Wideman et al., 1999) that culminates in hypoxemia and tissue hypoxia. This stimulates the proliferation of red blood cells, thereby increasing hematocrit values and blood viscosity (Maxwell et al., 1992; Shlosberg et al., 1996), eventually causing edema, accumulation of ascitic fluids in the abdominal cavity, and death.
The association between BW or the rate of weight gain (WG) and the incidence of AS (%AS) was investigated by exposing males from 6 commercial broiler crosses and 2 lines of label-type slow-growing broilers to a cold challenge (Gonzales et al., 1998). Mortality due to AS was found only among the fast-growing broiler crosses, compared with no %AS in the slow-growing lines. However, there was no correlation between mean growth rate and %AS among the 6 commercial broiler crosses, despite significant differences found in both traits. These findings indicate that AS develops only in broilers with a high growth rate but not at the same incidence in all of them. Wideman (1998) suggested that AS develops in broilers in which BW and WG exceeds the rate at which their pulmonary vascular capacity increases, but they do not necessarily have to be the fastest-growing birds in a flock. This hypothesis is best tested by comparing AS-susceptible and AS-resistant broilers within the same line rather than comparing between lines that were selected by different criteria over generations.
Several studies have reported moderate to high heritability for %AS in populations of fast-growing commercial broilers reared under low temperatures as AS-inducing conditions (AIC). Lubritz et al. (1995) found that this heritability ranged from 0.11 to 0.44. Similar results were reported by Moghadam et al. (2001), who estimated heritabilities of 0.22 and 0.41 in commercial populations of White Rock and Cornish males, respectively. Significant heritability of 0.25 (Lubritz et al., 1995), 0.54 (de Greef et al., 2001b), and 0.45 (Pakdel et al., 2002) has also been found for hypertrophy of the right ventricle, expressed as the elevated ratio of the weight of the right ventricle to the total ventricular weight (RV:TV); this ratio is regarded as being the most reliable indicator of AS (Julian, 1993; Lubritz et al., 1995; Wideman et al., 1998). These results suggest that direct selection against high %AS, or indirect selection for a lower RV:TV, may reduce %AS in commercial stocks of fast-growing broilers. However, to conduct a direct selection against %AS, the candidate birds must be exposed to AIC up to about 6 wk of age, to ensure mortality of all susceptible birds, as was done by Anthony and Balog (2003). Alternatively, all surviving birds need to be autopsied to determine their RV:TV. These procedures hinder the possibility of selecting the same candidate birds for the major broiler performance traits, such as growth rate and feed conversion. To integrate selection against AS into commercial breeding programs, one needs indicators of susceptibility to AS that are relatively noninvasive and can be measured in birds that are reared under standard conditions and hence remain healthy.
Many studies have focused on identifying reliable non-invasive physiological indicators for AS. Heart rate, measured by pulse oximetry or by electrocardiography, has been found to be lower in broilers suffering from AS than in their healthy counterparts (Kirby et al., 1997; Olkowski et al., 1997; Wideman et al., 1998). Olkowski et al. (2005) found that, at 35 d of age, the heart rate of broilers suffering from congestive heart failure, which is associated with hypoxemia and AS, was significantly lower than in healthy broilers. Broilers with AS have been found to have a significantly lower level of O2 saturation of hemoglobin in arterial blood (SaO2) than their healthy counter-parts at 6 wk of age (62.1 vs. 86.0%, respectively; Julian and Mirsalimi, 1992). Wideman and Kirby (1995a,b) found that broilers with AS, induced by pulmonary artery clamps, had a significantly lower SaO2 and a higher RV:TV when compared with non-AS healthy broilers. Mean hematocrit has also been found to be significantly higher in AS broilers than in their healthy counterparts reared under the same conditions (Julian and Mirsalimi, 1992; Maxwell et al., 1992; Lubritz and McPherson, 1994; Shlosberg et al., 1996; Wideman et al., 1998). Hematocrit has also been found to be highly heritable in broiler flocks reared under cold conditions (Shlosberg et al., 1996; de Greef et al., 2001b; Pakdel et al., 2002). Heritability has also been calculated for SaO2, with estimates ranging from about 0.5 (Druyan et al., 1999; Navarro et al., 2006) to 0.15 (de Greef et al., 2001b; Navarro et al., 2006).
In all of these studies, the physiological parameters were measured when the susceptible broilers had already started to develop AS. The heritability of these AS-related parameters supports the conclusion that susceptibility to AS is heritable (Pakdel et al., 2002, 2005b,Pakdel et al., c). However, the efficacy of these parameters as criteria for selecting against AS-susceptible individuals in a breeding program is limited (Balog, 2003), because if the selection candidates are kept under standard conditions, most of the susceptible individuals do not develop AS and hence are wrongly identified as being AS-resistant. Therefore, in the present study, growth and AS-related parameters were measured in young broilers kept at standard brooding conditions (SBC), under which no AS was recorded. Then, to identify AS-susceptible and AS-resistant individuals, all of the broilers were exposed to an efficacious AIC protocol. This design allowed us to fulfill the following objectives:
|
MATERIALS AND METHODS |
|---|
|
TOPABSTRACTINTRODUCTIONMATERIALS AND METHODSRESULTSDISCUSSIONREFERENCES |
|---|
The experimental population was derived from a broiler dam line (Anak Breeders Ltd., Netanya, Israel; ceased to exist in 2000). Each of 34 male parents (sires) was mated with 4 females (dams) to produce half-sib sire families. Male progeny from these families, 1 per dam, were tested in 2 replicated trials (trial 1 and trial 2).
Experimental Design
In trial 1, 136 male chicks (4 per sire) were brooded under SBC in a tiered brooder battery; in trial 2, 114 male chicks (3 to 4 per sire) were brooded under SBC on a concrete floor covered with wood shavings. At 19 d of age (d 19), the AIC protocol was instigated, whereby each chick was placed in an individual cage and exposed to lower-than-standard ambient temperatures (18 to 20°C) and high air velocity (about 3 m/s) induced by fans. Growth rate was enhanced by a modified feeding program, which consisted of a prestarter (d 0 to 4 instead of d 0 to 10), starter (d 5 to 14 instead of d 11 to 21), grower (d 15 to 24 instead of d 22 to 33), and finisher feed consisting of high-energy pelleted feed, from d 25 to 44. The contents of CP (%) and energy (kcal/kg of ME) in these 4 diets were as follows: 22 and 3,100, 20.5 and 3,125, 19.5 and 3,150, and 18.3 and 3,225, respectively. Feed and water were provided ad libitum. Growth rate was further enhanced by exposure to 23 h/d of light from hatch to the end of the trials on d 44.
Diagnosis of AS
Throughout the phase of AIC, all dead chicks were necropsied and examined to determine the cause of death. Chicks with ascitic fluid or hydropericardium were diagnosed as having died due to AS and were recorded as being AS-susceptible (SUS). The few birds that died from other causes were excluded from the data analyses. On d 44, all surviving birds were killed by cervical dislocation, necropsied, and visually examined. Birds with ascitic fluid or hydropericardium were diagnosed as exhibiting AS and were also recorded as SUS; all other birds were deemed healthy and noted as being AS-resistant (RES).
Measurements
BW and WG. Body weight was measured at least once a week, and the mean daily WG in each age interval (between 2 consecutive BW measurements) was calculated for each chick.
Hematocrit. Blood for hematocrit measurements was taken from a wing vein puncture into heparinized micro-capillary tubes and centrifuged in a microliter centrifuge (D-78532, Hettich Zentrifugen, Tuttlingen, Germany) for 7 min.
SaO2 and Heart Rate. Percentage saturation of hemoglobin with O2 in arterial blood (SaO2) and heart rate were measured using a portable veterinary oximeter (8600V, Nonin Medical Inc., Plymouth, MN) and a sensor (2000T, Nonin Medical Inc.). The sensor was placed over the cephalic vein of the right wing of lightly restrained birds held in lateral recumbency; SaO2 and heart rate were determined simultaneously, usually within 1 min. In the first week of life, a Nonin lingual sensor (2000SL, Nonin Medical Inc.) was used, positioned on the medial aspect of the thigh.
RV:TV. Hearts were collected from all chicks, those that died during the trials, and those killed at the end of the trials and were dissected to record the weight of the right ventricle and of the left ventricle + septum (total ventricle); the RV:TV ratio was calculated for each bird.
Statistical Analysis
Differences Between SUS and RES Chicks. Data from each trial were subjected to a separate 2-way AN-OVA according to the model
 | ([1]) |
with fixed effect of AS condition (SUS vs. RES) and random genetic effect of the sire. The interaction between these 2 effects could not be included, because some families had chicks from 1 phenotype only (all SUS or all RES).
Estimating Heritability.
The heritability estimates of BW, WG, hematocrit, SaO2, and heart rate were calculated only for measurements taken during the SBC period, because measurements taken under AIC were affected by development of AS in the SUS birds. Additionally, the number of SUS birds measured during this phase decreased with time (i.e., age) as more birds died from AS. The half-sib structure of the experimental population allowed estimations of heritability of the measured variables. The total phenotypic variance (VP) in the experimental population consisted of 2 variance components: between sire families (
2S) and within sire family [Residual, (2Res)]. The genetic expectation of 2S equals 25% of the additive genetic variance (
VA), whereas the genetic expectation of 2Res contains the remaining phenotypic variance: 75% of the additive genetic variance (
VA), the dominance variance (VD), and the environmental (nongenetic) variance (VE). Thus, estimates of narrow-sense heritability (h2n) were calculated by the following ratio:
 |
Standard errors of h2n estimates were calculated according to the formula 
, where T = the total number of progeny in all families (Falconer and Mackay, 1996).
The combined data of both trials were subjected to ANOVA according to the model
 | (4) |
with fixed effect of trial (1 or 2) and a random effect of sire nested within trial (Sire[Trial]). The variance component of Sire[Trial] provided the estimate of 2S, and the variance component of e estimated 2Res.
The heritability of AS was calculated according to the same model, but being a categorical variable (SUS or RES), it was estimated by GFCAT, software dedicated to the estimation of genetic parameters for categorical traits, named after the authors (Gianola and Foulley, 1983) of the theoretical framework (V. Ducrocq, INRA, Jouyen-Jasas Cedex, France, personal communication).
Genetic Correlation with %AS. Family means were calculated for each measurement. The data included a discrete variable for AS; each bird was assigned a value of 100 if it exhibited AS (SUS) or 0 if it was healthy (RES). Averaging this variable within families resulted in a continuous variable expressing the percentage of AS per family (%ASF). The estimates of pairwise correlation between %ASF and family means of the other measurements served as approximate estimates of genetic correlation between traits and were calculated separately from the data of each trial.
All statistical analyses were conducted using JMP software (SAS Institute, 2005). The method of restricted maximum likelihood was used to estimate variance components.
|
RESULTS |
|---|
|
TOPABSTRACTINTRODUCTIONMATERIALS AND METHODSRESULTSDISCUSSIONREFERENCES |
|---|
%AS. With 30% mortality and 14% morbidity, 44% of the birds developed AS (62/136 and 48/114 in trials 1 and 2, respectively), confirming the efficacy of the novel AIC protocol that was used in the present study. The values of %ASF ranged from 0 to 90%, and there was a significant correlation (r = 0.527; P = 0.014) between %ASF among progeny of the same sires in trials 1 and 2.
RV:TV.
The SUS chicks had significantly higher mean RV:TV ratios than the RES chicks in both trials, being 0.36 vs. 0.22 and 0.38 vs. 0.25 in trials 1 and 2, respectively (Table 1
).
|
). From d 29, i.e., 10 d after the birds were moved to AIC, mean WG was significantly lower in the birds that were developing AS (SUS) than in the healthy ones (RES), and the 2 groups differed accordingly in BW on d 35 and 42 (Table 2).
|
).
SaO2.
In both trials, when measured at the age of 7 d under SBC, the SUS chicks exhibited a slightly lower mean SaO2 than the RES chicks, but these differences were not significant (Table 1). Under AIC, the manifestations of AS in the SUS birds significantly reduced their mean SaO2 in trial 1 from 91.1 (d 7) to 87.9, 85.0, and 83.4% (d 25, 35, and 42, respectively) and in trial 2 from 95.6 (d 7) to 91.7, 83.1, and 78.4% (d 25, 35, and 42). A less-pronounced reduction with age in SaO2 was exhibited by the RES birds, and, consequently, the SUS and RES chicks differed significantly in mean SaO2 during the entire AIC phase.
Heart Rate.
Under SBC in both trials, the SUS chicks exhibited a slightly lower mean heart rate than the RES chicks, but the difference was significant only on d 15 in trial 1 (Table 1). After exposure to AIC, mean heart rate of the SUS birds was significantly lower than that of the RES birds, except from d 25 on in trial 2.
Heritability Estimates
Estimates of heritability for BW and WG, mostly similar across ages, ranged from 0.4 to 0.6 (Table 3). For hematocrit, the heritability was 0.39 on d 1 and 0.69 on d 16. Heritability of SaO2 on d 7 was 0.49, and for heart rate, the heritability was 0.46 on d 1 and 0.74 on d 15. Similar heritability (0.52) was estimated also for %AS, whereas a lower heritability (0.22) was estimated for the RV:TV ratio (Table 3).
|
A highly significant correlation (r = 0.561; P = 0.0035) was found between sire family means of RV:TV in trials 1 and 2, very similar to the correlation (r = 0.527) of %AS between sire families in the 2 trials. These similar correlations are in agreement with the significant correlations between %ASF and mean RV:TV, r = 0.781 (P < 0.0001) and r = 0.476 (P = 0.0251) in trials 1 and 2, respectively. These results indicate that also in the present study, RV:TV was a reliable indicator of AS, and therefore genetic association with AS manifestations was assessed by correlating family means of RV:TV (in addition to %ASF) with family means of all other traits.
Neither BW nor WG during the SBC phase were significantly correlated with %ASF or mean RV:TV in either trial (Table 4). Hematocrit was also not correlated with %ASF or RV:TV in either trial (Table 5). Family means of SaO2 on d 7 were negatively correlated with %ASF (r = –0.524 and –0.234 in trials 1 and 2, respectively) and with RV:TV (r = –0.618 and –0.510 in trials 1 and 2, respectively). Heart rate on d 1 was not correlated with %ASF or RV:TV in either trial. Heart rate on d 15 was significantly and similarly correlated with %ASF and RV:TV, except the correlations were negative in trial 1 (r = –0.323 and –0.299, respectively) and positive in trial 2 (r = 0.450 and 0.304, respectively; Table 5).
|
|
|
DISCUSSION |
|---|
|
TOPABSTRACTINTRODUCTIONMATERIALS AND METHODSRESULTSDISCUSSIONREFERENCES |
|---|
Whereas high rates of AS have been found under experimental conditions, AS mortality in commercial broiler flocks has been largely avoided in recent years by management that reduces the metabolic rate of the broilers and consequently their demand for O2 (Julian, 2000; Balog 2003). This is achieved by reducing the intake of dietary energy by using low-energy diets, by restricted feed consumption, e.g., by providing less hours of light per day, or both. Thus, although the genetic potential for rapid growth of commercial broilers has been continuously improved by breeding companies (Havenstein et al., 2003), its full expression is not allowed at the farm level, to avoid morbidity and mortality of AS-susceptible birds. A better solution would be to select against AS susceptibility, because if all broilers were resistant to AS, management-induced reduction of growth rate would no longer be needed. However, the breeding approach is feasible only if there is a heritable susceptibility to AS and if an efficacious selection against it can be performed.
Several studies (Lubritz et al., 1995; de Greef et al., 2001a; Moghadam et al., 2001; Pakdel et al., 2002; Anthony and Balog, 2003) have shown that the %AS in populations of commercial broilers is under genetic control, with heritability estimates ranging from 0.11 to 0.44. The results of the present study are in agreement with these previous studies, but with a higher estimate of heritability (0.52), possibly reflecting the higher %AS due to the more efficacious AIC protocol that was used. The hereditary nature of AS was also evidenced by the highly significant correlation between trials 1 and 2 in %ASF and in family means of RV:TV. These results clearly indicate that a substantial portion of the variation among families in %ASF, ranging from 0 to 90%, was a genetic variation. The reliability of the genetic information on AS obtained in this study was indicated by the high estimates of heritability (0.4 to 0.6) of BW and WG measured under SBC, which are in agreement with numerous previous reports (Lubritz et al., 1995; Pakdel et al., 2002, 2005b, Pakdel et al., c). Similar means of BW and WG were exhibited, throughout the entire SBC phase, by the birds that later developed AS (SUS group) and those that remained healthy under AIC (RES group). These results, and the lack of genetic correlation between obvious AS parameters (%ASF and RV:TV) and early WG and BW, indicate that within the tested stock, there was no association between susceptibility to AS and variation in early growth rate. Therefore, in such a broiler stock, further selection for a more rapid growth is not expected to increase %AS. Nevertheless, selection against susceptibility to AS should be incorporated into commercial breeding programs to reduce the frequency of AS-susceptible individuals, provided that they can be reliably identified for selection.
Mortality or morbidity due to AS provides the ultimate identification of AS-susceptible individuals (Julian, 2000). However, actual development of AS in susceptible birds depends on environmental conditions that increase O2 deficiency, either by reducing the supply of O2 or by increasing the demand for (and use of) O2 (Balog, 2003). Anthony and Balog (2003) found that a hypobaric chamber with a reduced partial pressure of O2 simulating that at 2,900 m above sea level successfully induced 66% AS in a commercial sire line. Cisar et al. (2003) found that in 6 lines of commercial broilers that were reared in the same hypobaric chamber, 47% of the birds developed AS. Thus, the hypobaric chamber has proved to be a useful tool for AS research, but due to its high cost and limited capacity, it is not suitable for large-scale studies or for commercial selection against AS susceptibility. Wideman and Kirby (1995a,b) found that clamping the left pulmonary artery induced around 70% AS among commercial broilers. Wideman et al. (1997) also found that a second surgical procedure, involving unilateral occlusion of the primary bronchus, induced 31% AS in a commercial parental broiler line (Wideman and French, 2000). Both methods are invasive, require surgical skills, and are time-consuming and are therefore less feasible for practical breeding against susceptibility to AS or for large-scale AS research. More recently, Wideman and Erf (2002) used injection of microparticles as an experimental model to induce AS. Cold stress has been used to induce AS in most studies in which many birds were tested, resulting in a lower %AS. Pakdel et al. (2005b) reported 16% AS among broilers that had been gradually exposed to cold, with ambient temperatures decreasing from 30°C on d 1 to 10°C at d 22. De Greef et al. (2001b) found that similar exposure, with ambient temperature declining to 15°C at d 16, induced AS among broilers from 10 lines at rates ranging from 1 to 20%. Shlosberg et al. (1996, 1998) obtained similar rates of AS mortality in broiler flocks exposed to cold winter conditions in Israel. These results suggest that low ambient temperatures induce AS only in a portion of the susceptible individuals, whereas the other susceptible birds escape the cold stress, probably by congregating together and due to the insulating effects of the litter and the heat produced by microbial fermentation in the litter.
In the present study, a novel AIC protocol was developed. Reared in individual cages from 19 d of age, the tested birds could not escape the challenge of the environmental conditions, consisting of fan-induced air movement (about 3 m/s) and moderately low ambient temperatures (18 to 20°C). The environmental conditions were augmented by early use of high-energy pelleted feed to enhance rapid growth and by 23 h/d of light. Under these combined conditions, %AS among the broilers in the present study was 44%, much higher than those reported for cold-stressed broilers on litter and similar or slightly lower than %AS among broilers challenged by hypobaric chamber or by surgical treatments. It appears that the AIC protocol of individual cages that was used in the present study can induce AS in probably all (or most of) the genetically susceptible broilers. This emphasizes the relevance of the findings reported here, compared with studies with substantially lower rates of AS.
The successful induction of AS in this study suggests that breeding for AS resistance can be conducted by keeping all selection candidates under AIC that eliminate all susceptible individuals. This was done successfully by Wideman and French (2000), but on an experimental scale. However, such direct selection cannot be applied in commercial breeding programs, because it compromises the selection for more important traits, such as growth rate and meat yield. Specific indicator(s) of AS susceptibility (or resistance), once found, could facilitate indirect selection against AS susceptibility integrated into a multitrait breeding program of commercial broilers (Balog, 2003). To be a useful selection criterion, such an indicator should be heritable and truly genetically associated with AS resistance or susceptibility; expressed in broilers under standard conditions, thus allowing all of them to fully express their genetic potential in all traits; and easy to measure, to facilitate selection in large populations with minimal costs.
Many studies have investigated AS-related traits, and a few of them have estimated the heritability of those traits and their genetic correlation with AS (Lubritz and McPherson, 1994; Lubritz et al., 1995; Pakdel et al., 2005a,b,c; Zerehdaran et al., 2006). Other studies have looked for differences in those traits between broilers developing AS and healthy ones (Julian and Mirsalimi, 1992; Maxwell et al., 1992; Shlosberg et al., 1996; Kirby et al., 1997; Olkowski et al., 1997, 2005; Wideman et al., 1998; de Greef et al., 2001a; Luger et al., 2001). In the present study, too, means of the birds with AS differed significantly from the healthy ones (higher RV:TV and hematocrit; lower heart rate, SaO2, WG, and BW) when measured after AS started to develop, i.e., under AIC. However, all of these differences were secondary manifestations of the developing AS, whereas a useful indicator should significantly differ between AS-susceptible and AS-resistant individuals when reared under standard rearing conditions.
The unique design of the present study allowed us to measure AS-related traits in all chicks during the first 18 d under SBC and then distinguish between the susceptible and resistant individuals by moving them to AIC, which effectively induced AS in the susceptible birds. In this design, a trait measured under SBC and differing significantly between the susceptible and resistant birds, and found to be heritable and genetically correlated with AS, is expected to be a good indicator for selection against AS susceptibility. Significant heritability was found for all of the traits measured under SBC. However, hematocrit measured under SBC (on d 1 and 16) was not associated with %ASF under AIC. Heart rate was slightly lower under SBC (on d 1 and 15) in the SUS chicks than in the RES chicks, but the difference was significant only in trial 1. Additionally, the genetic correlation between heart rate and %ASF was neither significant nor consistent in the 2 trials. Therefore, heart rate and hematocrit did not appear to be adequate indicators for selection against AS susceptibility under SBC. Mean SaO2 on d 7 was only slightly lower in the SUS birds than in the RES ones, suggesting no (or weak) phenotypic association with AS. However, family means of SaO2 at these early ages exhibited consistent significant negative genetic correlation with both %ASF and RV:TV. Low SaO2 was suggested as a reliable early genetic indicator for AS susceptibility (Druyan et al., 1999). In recent years, some breeding companies have selected against broilers with low SaO2, as measured in selection candidates at 5 wk of age (Navarro et al., 2006). However, due to the low %AS in these unstressed flocks, high SaO2 levels are expected in susceptible individuals that do not develop AS. Navarro et al. (2006) reported a low heritability (0.15) for SaO2 at 5 wk of age in commercial breeding lines. Due to this low heritability, and only moderate genetic correlation with actual manifestation of AS, the effectiveness of 5-wk SaO2 as an indicator for selection against AS susceptibility must be limited.
In conclusion, the results of the present study suggest that although all traits measured were significantly heritable and hence can be altered by selection, only low SaO2 may potentially serve as an early criterion for selection against AS susceptibility, albeit with limited efficacy. It appears that a primary indicator of AS was not identified in the present study, either because it was not measured or because it was already manifested in the embryo or in a very early postnatal phase, when the cardiovascular system is developed and has started functioning. However, measurements of physiological functions at the embryonic stage or in very young chicks are often lethal in nature, and hence it is not possible to later determine under AIC if each individual was susceptible or resistant to AS. To overcome this limitation, advanced research aimed at detecting inherent primary indicators of AS should consist of functional or molecular comparisons between embryos or chicks from 2 genetically divergent lines in which the individuals are either all AS-susceptible or all AS-resistant.
|
ACKNOWLEDGMENTS |
|---|
Received for publication October 16, 2006. Accepted for publication November 19, 2006.
|
REFERENCES |
|---|
|
TOPABSTRACTINTRODUCTIONMATERIALS AND METHODSRESULTSDISCUSSIONREFERENCES |
|---|
Balog, J. M. 2003. Ascites syndrome (pulmonary hypertension syndrome) in broiler chickens: Are we seeing the light at the end of the tunnel? Avian Poult. Biol. Rev. 14:99–126.
Cisar, C. R., J. M. Balog, N. B. Anthony, and A. M. Donoghue. 2003. Sequence analysis of bone morphogenetic protein receptor type II mRNA from ascitic and nonascitic commercial broilers. Poult. Sci. 82:1494–1499.
Currie, R. J. 1999. Ascites in poultry: Recent investigations. Avian Pathol. 28:313–326.[Web of Science][Medline]
Decuypere, E., J. Buyse, and N. Buys. 2000. Ascites in broiler chickens: Exogenous and endogenous structural and functional causal factors. World’s Poult. Sci. J. 56:367–377.
de Greef, K. H., L. L. Janss, A. L. Vereijken, R. Pit, and C. L. Gerritsen. 2001a. Disease-induced variability of genetic correlations: Ascites in broilers as a case study. J. Anim. Sci. 79:1723–1733.
de Greef, K. H., C. Kwakernaak, B. J. Ducro, R. Pit, and C. L. Gerritsen. 2001b. Evaluation of between-line variation for within-line selection against ascites in broilers. Poult. Sci. 80:13–21.
Druyan, S., A. Cahaner, M. Bellaiche, A. Rosner, and A. Shlosberg. 1999. Genetics of blood oxygenation, heart rate, and ECG waveforms, and their association with ascites in broilers. Page 112 in Proc. 1st Eur. Poult. Genet. Symp., Mariensee, Germany. World’s Poult. Sci. Assoc., Mariensee, Germany.
Falconer, D. S., and T. F. C. Mackay. 1996. Introduction to Quantitative Genetics. 4th ed. Longman Group Ltd., Harlow, UK.
Gianola, D., and J. L. Foulley. 1983. Sire evaluation for ordered categorical trait with a threshold model. Genet. Sel. Evol. 15:201–224.
Gonzales, E., L. Buyse, T. S. Takita, J. R. Sartori, and E. Decuypere. 1998. Metabolic disturbances in male broilers of different strains. 1. Performance, mortality, and right ventricular hypertrophy. Poult. Sci. 77:1646–1653.
Hadad, Y., S. Druyan, and A. Cahaner. 2006. Ascites in commercial broilers—is it associated with rapid growth? World’s Poult. Sci. J. 62(Suppl.):602–603. (Abstr.)
Havenstein, G. G., P. R. Ferket, and M. A. Qureshi. 2003. Carcass composition and yield of 1957 versus 2001 broilers when fed representative 1957 and 2001 broiler diets. Poult. Sci. 82:1509–1518.
Julian, R. J. 1993. Ascites in poultry. Avian Pathol. 22:419–454.
Julian, R. J. 2000. Physiological, management and environmental triggers of the ascites syndrome: A review. Avian Pathol. 29:519–527.
Julian, R. J., and S. M. Mirsalimi. 1992. Blood oxygen concentration of fast-growing and slow-growing broiler chickens, and chickens with ascites from right ventrical failure. Avian Dis. 36:730–732.[Web of Science][Medline]
Kirby, Y. K., R. W. McNew, J. D. Kirby, and R. F. Wideman Jr. 1997. Evaluation of logistic versus linear regression models for predicting pulmonary hypertension syndrome (ascites) using cold exposure or pulmonary artery clamp models in broilers. Poult. Sci. 76:392–399.
Lubritz, D. L., and B. N. McPherson. 1994. Effect of genotype and cold stress on incidence of ascites in cockerels. J. Appl. Poult. Res. 3:171–178.
Lubritz, D. L., J. L. Smith, and B. N. McPherson. 1995. Heritability of ascites and the ratio of right to total ventricle weight in broiler breeder male lines. Poult. Sci. 74:1237–1241.[Web of Science][Medline]
Luger, D., D. Shinder, V. Rzepakovsky, M. Rusal, and S. Yahav. 2001. Association between weight gain, blood parameters, and thyroid hormones and the development of ascites syndrome in broiler chickens. Poult. Sci. 80:965–971.
Maxwell, M. H., G. W. Robertson, and C. C. McCorquodale. 1992. Whole blood and plasma viscosity values in normal and ascetic broiler chickens. Br. Poult. Sci. 33:871–877.[Web of Science][Medline]
Moghadam, H. K., I. McMillan, J. R. Chambers, and R. J. Julian. 2001. Estimation of genetic parameters for ascites syndrome in broiler chickens. Poult. Sci. 80:844–848.
Navarro, P., P. M. Visscher, D. Chatziplis, A. N. Koerhuis, and C. S. Haley. 2006. Segregation analysis of blood oxygen saturation in broilers suggets a major gene influence on ascites. Br. Poult. Sci. 47:671–684.[Web of Science][Medline]
Olkowski, A. A., J. A Abbott, and H. L. Classen. 2005. Pathogenesis of ascites in broilers raised at low altitude: Aetiological considerations based on echocardiographic findings. J. Vet. Med. Ser. A Physiol. Pathol. Clin. Med. 52:166–171.
Olkowski, A. A., H. L. Classen, C. Riddell, and D. Bennett. 1997. A study of electrocardiographic patterns in a population of commercial broiler chickens. Vet. Res. Commun. 21:51–62.[Web of Science][Medline]
Pakdel, A., P. Bijma, B. J. Ducro, and H. Bovenhuis. 2005a. Selection strategies for body weight and reduced ascites susceptibility in broilers. Poult. Sci. 84:528–535.
Pakdel, A., J. A. Van Arendonk, A. L. Vereijken, and H. Bovenhuis. 2002. Direct maternal genetic effect for ascites-related traits in broilers. Poult. Sci. 81:1273–1279.
Pakdel, A., J. A. Van Arendonk, A. L. Vereijken, and H. Bovenhuis. 2005b. Genetic parameters of ascites-related traits in broilers: Effect of cold and normal temperature conditions. Br. Poult. Sci. 46:35–42.[Web of Science][Medline]
Pakdel, A., J. A. Van Arendonk, A. L. Vereijken, and H. Bovenhuis. 2005c. Genetic parameters of ascites-related traits in broilers: Correlations with feed efficiency and carcass traits. Br. Poult. Sci. 46:43–53.[Web of Science][Medline]
SAS Institute. 2005. JMP Version 6 User’s Guide. SAS Inst. Inc., Cary, NC.
Shlosberg, A., M. Bellaiche, E. Berman, S. Perk, N. Deeb, E. Neumark, and A. Cahaner. 1998. Relationship between broiler chicken haematocrit-selected parents and their progeny, with regard to haematocrit, mortality from ascites and bodyweight. Res. Vet. Sci. 64:105–109.[Web of Science][Medline]
Shlosberg, A., M. Bellaiche, G. Zeitlin, M. Ya’acobi, and A. Cahaner. 1996. Hematocrit values and mortality from ascites in cold-stressed broilers from parents selected by hematocrit. Poult. Sci. 75:1–5.[Web of Science][Medline]
Wideman, R. F., Jr. 1998. Causes and control of ascites in broilers. Pages 56–85 in Proc. Natl. Meet. Poult. Health Process. Georgetown, DE. Delmarva Poult. Ind. Inc., Georgetown, DE.
Wideman, R. F., Jr. 2001. Pathophysiology of heart/lung disorders: Pulmonary hypertension syndrome in broiler chickens. World’s Poult. Sci. J. 57:289–307.
Wideman, R. F., and G. F. Erf. 2002. Intravenous micro-particle injection and pulmonary hypertension in broiler chickens: Cardio-pulmonary hemodynamic responses. Poult. Sci. 81:877–886.
Wideman, R. F., Jr., and H. French. 2000. Ascites resistance of progeny from broiler breeders selected for two generations using chronic unilateral pulmonary artery occlusion. Poult. Sci. 79:396–401.
Wideman, R. F., Jr., and Y. K. Kirby. 1995a. A pulmonary artery clamp model for inducing pulmonary hypertension syndrome (ascites) in broilers. Poult. Sci. 74:805–812.[Web of Science][Medline]
Wideman, R. F., Jr., and Y. K. Kirby. 1995b. Evidence of a ventilation perfusion mismatch during acute unilateral pulmonary artery occlusion in broilers. Poult. Sci. 74:1209–1217.[Web of Science][Medline]
Wideman, R. F., Jr., Y. K. Kirby, R. L. Owen, and H. French. 1997. Chronic unilateral occlusion of an extrapulmonary primary bronchus induces pulmonary hypertension syndrome (ascites) in male and female broilers. Poult. Sci. 76:400–404.
Wideman, R. F., Jr., P. Maynard, and W. G. Bottje. 1999. Venous blood pressure in broilers during acute inhalation of five percent carbon dioxide or unilateral pulmonary artery occlusion. Poult. Sci. 78:1443–1451.
Wideman, R. F., Jr., T. Wing, Y. K. Kirby, M. F. Forman, N. Marson, C. D. Tackett, and C. A. Ruiz-Feria. 1998. Evaluation of minimally invasive indices for predicting ascites susceptibility in three successive hatches of broilers exposed to cool temperatures. Poult. Sci. 77:1565–1573.
Zerehdaran, S., E. M. van Greehof, E. H. van der Waaij, and H. Bovenhuis. 2006. A bivariate mixture model analysis of body weight and ascites traits in broilers. Poult. Sci. 85:32–38.
This article has been cited by other articles:
|
|
 |
|
  S. Druyan, D. Shinder, A. Shlosberg, A. Cahaner, and S. Yahav Physiological parameters in broiler lines divergently selected for the incidence of ascites Poult. Sci., September 1, 2009; 88(9): 1984 - 1990. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
A. M. Closter, P. van As, M. A. M. Groenen, A. L. J. Vereijken, J. A. M. van Arendonk, and H. Bovenhuis Genetic and phenotypic relationships between blood gas parameters and ascites-related traits in broilers Poult. Sci., March 1, 2009; 88(3): 483 - 490. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
D. Shinder, M. Rusal, M. Giloh, and S. Yahav Effect of repetitive acute cold exposures during the last phase of broiler embryogenesis on cold resistance through the life span Poult. Sci., March 1, 2009; 88(3): 636 - 646. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
S. Druyan, Y. Hadad, and A. Cahaner Growth Rate of Ascites-Resistant Versus Ascites-Susceptible Broilers in Commercial and Experimental Lines Poult. Sci., May 1, 2008; 87(5): 904 - 911. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
S. Druyan and A. Cahaner Segregation Among Test-Cross Progeny Suggests That Two Complementary Dominant Genes Explain the Difference Between Ascites-Resistant and Ascites-Susceptible Broiler Lines Poult. Sci., November 1, 2007; 86(11): 2295 - 2300. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
S. Druyan, A. Ben-David, and A. Cahaner Development of Ascites-Resistant and Ascites-Susceptible Broiler Lines Poult. Sci., May 1, 2007; 86(5): 811 - 822. [Abstract] [Full Text] [PDF]
|
|
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
