Relevance of Rapid Growth in Broilers to Management and Genetic Aspects of the Ascites Syndrome

The susceptibility of broilers to ascites syndrome is a genetic ‘defect’, which is not genetically correlated with growth rate and so selection against susceptibility to the syndrome is recommended, Avigdor Cahaner of the Hebrew University in Israel told the Australian Poultry Science Symposium 2011.
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Modern broilers are characterized by high growth rate (GR), high rate of feed intake and metabolism and increased oxygen demand. Cold stress increases oxygen demand and those broilers that fail to fully supply it develop the ascites syndrome (AS), which is induced also at high altitudes where low oxygen availability is the stressor. The development of AS can be avoided by reducing GR, but with longer rearing period and often poorer feed conversion. The susceptibility of broilers to AS is a genetic ‘defect’ which is not genetically correlated with GR, hence selection against AS susceptibility is recommended. Such selection will be enhanced by the expected use of genomic markers linked to AS-controlling genes.


Rapid growth, due to the consequent shorter rearing time to marketing and favorable feed conversion ratio (FCR), is the main factor contributing to economically efficient broiler production. Accordingly, commercial breeding programs have been continuously selecting for high growth rate (GR) and achieved outstanding progress in developing fast-growing meat-type broiler chickens. These achievements were clearly demonstrated in two similar trials, conducted by Havenstein and co-workers in the years 1991 and 2001, where the contemporary broilers reach market body weight (BW) in fewer days, with a superior FCR (Havenstein et al., 1994, 2003).

The higher GR of contemporary broilers is driven by a higher feed intake per time-unit and higher metabolic rate, and consequently a higher demand for oxygen, beginning from the embryonic stage (Tona et al., 2004). Higher metabolic rate, especially when coupled with exposure to low ambient temperatures or lower availability of oxygen (high-altitude rearing), leads to reduced capability of some broilers to regulate oxygen supply and energy balance (Wideman et al., 1999), leading to development of the ascites syndrome (AS) that results in eventual mortality (Julian, 1993; 2000, Wideman, 1998).

The higher GR of contemporary broilers is driven by a higher feed intake per time-unit and higher metabolic rate, and consequently a higher demand for oxygen, beginning from the embryonic stage (Tona et al., 2004). Higher metabolic rate, especially when coupled with exposure to low ambient temperatures or lower availability of oxygen (high-altitude rearing), leads to reduced capability of some broilers to regulate oxygen supply and energy balance (Wideman et al., 1999), leading to development of the ascites syndrome (AS) that results in eventual mortality (Julian, 1993; 2000, Wideman, 1998).

Genetic and Breeding Aspects of the Ascites Syndrome (AS)

Management approaches to reduce the incidence of AS

In the 1970’s, AS was observed among broilers reared at the Andes high altitudes (Cueva et al., 1974), and later in South Africa (Huchzermeyer et al., 1988). Since the 1990s, following the continuous genetic improvement in broilers’ growth rate (GR), AS had been found also at low altitudes (Albers and Frankenhuis, 1990), mainly among broilers reared at low ambient temperatures and/or fed high-energy pelleted feed. Management schemes have been applied since the 1990’s to avoid or minimize AS mortality: (1) increasing broiler-house temperature by costly heating and insulation, (2) slowing actual GR, and consequently reducing metabolic rate and demand for oxygen. The latter can be achieved by feed restriction (FR) – either by restricting the daily feed ration or by providing less hours of light to reduce actual daily feed consumption, or by low-energy mash feeds to reduce intake of dietary energy (Balog 2003; Julian 2000).

The relative effects of heating and FR on the development of AS were investigated in broilers at high altitude, reared at cold vs. normal ambient temperature (Ta), and three feeding regimes (Ozkan et al., 2010). In the cold conditions, Ta ranged between 16 to 17°C in the 4th week, 17 to 19°C in the 5th week and 19 to 21°C thereafter. In the normal conditions, Ta was 24°C in the 4th week and ranged between 22 to 24°C thereafter.

Broilers in each condition were divided into three groups: FR from 7 to 14 days (FR7-14); FR from 7 to 21 days (FR7-21); and ad libitum (AL). Mortality due to AS and related parameters were recorded.

Under normal Ta, AS mortality was lower in females (8.6 per cent) than in males (13.8 per cent) and was not affected by the feeding regime. Under cold Ta, there was higher AS mortality, but only in males; it was 44.2 per cent among AL-fed males and only about 26 per cent under the FR regimens, suggesting that FR helped some males to better acclimatize to the cold Ta and avoid AS. However, mortality was only 13.3 per cent in AL-fed males at normal Ta and FR did not further reduce the incidence of ascites under these conditions. Thus, avoiding cold Ta in the poultry house by slight heating was more effective than FR in reducing ascites mortality.

However, all management approaches to reduce the incidence of AS compromise the efficacy of broiler production. If feed restriction is applied to reduce growth rate, the broilers do not fully express their genetic potential for rapid growth, and consequently production costs are increased due to longer period of rearing to marketing bodyweight (BW), poorer feed conversion, and less efficient use of labour and facilities. Extra heating and insulation also increase production costs. Therefore the following parts of this paper deal with the genetic approach to overcome AS susceptibility of high-GR broilers. Compared to the management approaches, breeding provides a sustainable solution the AS problem, but it is feasible only if there is an inherent susceptibility to AS, and if effective selection against it can be performed.

High GR and the incidence of AS are associated phenotypically

Contemporary commercial broilers were compared in 1991 with a control population representing commercial broilers of 1957 (Havenstein et al., 1994). Average daily BW gain of the 1957 and 1991 broilers were 10 versus 31g per day from hatch to three weeks of age, respectively, and 19 versus 68g per day from three to six weeks. The tremendous increase in GR coincided with a cumulative mortality of 14.1 per cent in the 1991 broilers, mainly due to AS, whereas the 1957 broilers had a cumulative mortality of only 2.8 per cent, with no cases of AS. Based on these findings, the authors suggested that AS developed due to the selection for higher GR, because it occurred without concomitant development in efficacy of the cardiovascular and respiratory systems.

In a pedigree population of commercial broiler line with a wide genetic variation for GR, AS per sire family among progeny exposed to ascites-inducing conditions (AIC) was positively correlated with GR of their sibs under normal conditions (Deeb et al., 2002). Also Moghadam et al. (2001) found a positive genetic correlation between the tendency of broilers to develop AS and their BW under normal climatic conditions. Several earlier publications stating that AS develops in individuals with more rapid early growth were reviewed by Julian (1998, 2000). These findings led to the suggestion that further enhancement of broilers’ GR, either by selective breeding or by advanced management, should be avoided as it will increase the incidence of AS in contemporary broiler flocks.

Results from a study with six high-GR broiler crosses and two lines of ‘Label—-type slow-growing broilers indicated that AS develops only in fast-growing broiler lines but not at the same incidence in all of them (Gonzales et al., 1998). It was suggested that AS develops in broilers in which GR 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 was supported by Decuypere and Buyse (2005) who stated that AS is caused by an impaired oxygen supply that cannot sustain the rapid growth, rather than by increased oxygen requirement per se.

High GR and the incidence of AS are not correlated genetically

Due to the association between high GR, oxygen demand, and AS, it has been suggested that AS is induced by high GR. If true, further GR enhancement should be avoided as it will increase the proportion of AS-susceptible individuals in contemporary stocks. An alternative hypothesis claims that AS is associated with high actual GR only because the latter increases oxygen demand and that there are genetically AS-resistant broilers that do not develop AS even when exhibiting high GR. These two hypotheses were tested in trials in the years 2002 and 2006, with contemporary fast-growing commercial broiler lines and an experimental line derived from commercial broilers in the year 1986 (Druyan et al., 2008). A protocol of high-challenge ascites-inducing conditions (AIC) from day 19 was used to distinguish between AS-susceptible and AS-resistant individuals and to determine their GR to this age.

In the high-GR broiler lines, AS incidence was 31 per cent and 47 per cent in 2002 and 2006, respectively, and 32 per cent in the 1986 slow-growing line. Most broilers that remained healthy under the high-challenge AIC exhibited the same early GR and BW as those that later developed AS. These results, and the relatively high incidence of AS in the slow-growing line, indicate that there is very little if any direct genetic association between AS and genetic differences in potential GR, and suggest that AS-resistant broilers can be selected for higher GR and remain healthy even under AIC.

In another study with contemporary commercial broilers, all the chicks were reared under standard conditions to day 19, and thereafter exposed to AIC that effectively induced AS in all the susceptible individuals (Druyan et al., 2007a). This experimental procedure revealed that the GR up to day 19 of the broilers that later developed ascites was similar to the GR of their counterparts that remained healthy, suggesting that within that study’s population, high early GR was not associated with susceptibility to AS. In another trial by Druyan et al. (2007b), about 250 broilers that later developed AS, and about 650 broilers that remained healthy to day 49, all reared together under moderate-challenge AIC, exhibited similar GR until day 17.

Similar results were obtained in two recent trials in Ecuador; broilers from two commercial breeds were reared at high altitude (2400 metres) under management that allows maximal GR (pelleted feed and 22 hours per day of light). The incidence of AS ranged among the breed-by-sex groups, from eight per cent to 57 per cent. However, in all groups, the range and mean of BW on day 21 (before AS effects on BW were apparent) were similar in the broilers that later died due to AS and their counterparts that remained healthy to the end of the trial at the 7th week (Romo and Kalinowski, unpublished data). Based on these results, it appears that the genetic variation in susceptibility to AS is not associated with GR variation in modern commercial broiler breeds. Accordingly, the continuous genetic enhancement of GR has not increased the proportion of AS-susceptible individuals in modern broiler stocks; it is the higher GR and the consequent higher oxygen demand that trigger AS development in a larger proportion of the AS-susceptible individuals in these stocks. This conclusion was supported by a study where genetically slow-growing broilers were exposed to high-challenge AS inducing conditions for 54 days, and eventually 30 per cent of them developed AS (Druyan et al., 2008).

Genetic control of susceptibility to AS

Several studies found a genetic component in broilers’ tendency to develop AS, with heritability estimates from 0.11 to 0.44 (Lubritz and McPherson, 1994; Lubritz et al., 1995; Moghadam et al., 2001; Pakdel et al., 2005; Druyan et al., 2007a,b; Pavlidis et al., 2007). Wideman and French (2000) suggested that gene or genes were involved in the response to their successful two–cycle selection against AS susceptibility. Single gene inheritance was suggested also by Navarro et al. (2005). These authors performed a complex segregation analysis of data on oxygen saturation of the haemoglobin in arterial blood (SaO2), a trait known to be closely related to AS (Druyan et al., 2007a). Data on SaO2 from 12,000 males in fully pedigreed populations of an elite male line that has been closed for about 35 generations were available for that study. The results suggested that a single di-allelic dominant locus was responsible for 90 per cent of the genetic variation in SaO2, with high levels of SaO2 indicating AS resistance, whereas low levels indicated AS susceptibility. Druyan et al. (2007b) noted that the extremely rapid divergence between their selected AS-S and AS-R lines may suggest the involvement of one or several major genes. Moreover, analysis of AS segregation within families in the selected lines suggested dominance of AS resistance.

Most studies considered AS susceptibility as a polygenic trait (e.g., Moghadam et al., 2001; Pakdel et al. 2005) but they were conducted under low-challenge AIC, where birds with relatively low GR, hence low oxygen demand, do not develop AS even if they are genetically susceptible. Therefore under such conditions, genes that affect GR are indirectly affecting the development of AS in the genetically susceptible birds. This situation, which apparently was common in many studies on the genetics of AS, complicated the efforts to select against AS susceptibility and to identify the genes with direct effect on AS. The studies of Wideman and French (1999, 2000), Pavlidis et al. (2007), and ours (Druyan and Cahaner, 2007; Druyan et al., 2007a,b; 2008;) were conducted under high-challenge AIC protocol. Under such conditions, all AS susceptible birds develop AS, even those with lower growth rate, thus facilitating the conclusion that only a few major genes are directly responsible for AS susceptibility.

Direct selection against susceptibility to AS

Successful selection against AS susceptibility was conducted by Wideman and French (1999, 2000) in a full-pedigreed elite commercial broiler breeder line. They used for reproduction only males and females that did not develop AS following AS-inducing surgery (unilateral pulmonary artery occlusion). After 2 cycles of such selection, per centAS among males that were exposed to cool temperatures (14°C) from 17 to 49 days of age, was reduced to four per cent, compare to 15 per cent after one cycle of this selection, and 31 per cent in the base population. That study demonstrated the feasibility of selection based on mortality of AS-susceptible individuals under a protocol of high-challenge AIC. Divergent selection for AS mortality was conducted by Anthony and co-workers (Pavlidis et al., 2007). The AS was induced in a hypobaric chamber where oxygen content was reduced to the level of 2,900 metres above sea level. After 10 generations of divergent sire-family selection, AS increased to about 90 per cent in the AS-susceptible line and decreased to about 20 per cent in the AS-resistant line, thus reaching a divergence of about 70 per cent (Pavlidis et al., 2007).

Similarly successful divergent selection was applied by Druyan et al. (2007b). The first selection cycle was based on progeny testing for AS mortality under low-challenge AIC. Two additional cycles of full-pedigree progeny testing were conducted under high-challenge AIC protocol (Druyan et al., 2007a,b). Two divergent lines were established, AS-susceptible (AS-S) and AS-resistant (AS-R), with respectively 95 per cent and 5 per cent of AS (a divergence of 90 per cent) when reared together under the same high-challenge AIC (Druyan et al, 2007b).

Indirect selection against susceptibility to AS

In order to conduct effective selection on AS mortality, the candidate birds must be exposed to extreme AIC up to about six weeks. This has been done in all the experimental selection projects mentioned in Section e, in order to assure that all the genetically susceptible birds develop AS, because under standard broiler conditions only few individuals – is at all – develop AS. Keeping the candidate birds under extreme AIC precludes the possibility to select them for normal broiler performance traits. Therefore, it is important to find indicators of broilers’ susceptibility to AS, that can be measured on birds under standard broiler conditions; such indicators allow the integration of indirect selection against AS susceptibility into the standard breeding programs of commercial broiler stocks. Many studies (reviewed by Druyan et al., 2007a) found significant physiological differences between broilers with AS versus healthy ones. However, in all these studies, the physiological variables were measured at the phase when the susceptible broilers had already started to develop AS. Hence, these variables cannot serve as indicators of AS-susceptibility under normal conditions at early ages (at hatching or during the brooding period).

The exact initial biochemical and physiological factors related to the genetic propensity to develop AS are still not known. It is often difficult to prove that a particular change is primary in nature, and so determinative, or is a subsequent secondary manifestation in the development of AS. If specific parameters to predict AS susceptibility or resistance are sought, it is of paramount importance that the primary changes be determined and evaluated. Moreover, in order to assess their significance as criteria for selection, it is necessary to estimate the heritability of these parameters, and their genetic correlation to consequent AS development under AIC.

Genomic selection against susceptibility to AS

Data from test-crosses between our fully-divergent AS-S and AS-R lines suggested that only two major genes control this genetic divergence (Druyan and Cahaner, 2007). If indeed only few genes are involved in the genetic control of susceptibility to AS, and given the current rapid advancement of genomic tools, the AS genes should be detected and mapped in the near future (if not mapped already by the breeding companies). Once mapped, with the help of current and future genomic methodologies, the causative SNPs (or closely linked ones, as markers) in these genes will be identified. High-throughput genomic asseys may soon facilitate efficient genotyping of these marker SNPs, and their routine utilization in commercial breeding programs. With such markers, high-challenge AIC is not needed to effectively select against susceptibility to AS, because breeders will be able to easily detect and cull individual birds, within the elite lines, that carry the alleles for AS susceptibility. All major broiler breeding companies have been heavily involved in R&D efforts aimed at achieving this goal.


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Further Reading

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March 2011
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