British Poultry Science Volume 46, Number 1 (February 2005), pp.

54–57

Heritability of sudden death syndrome and its associated correlations

to ascites and body weight in broilers
H.K. MOGHADAM, I. MCMILLAN, J.R. CHAMBERS1, R.J. JULIAN2
3
AND C.C. TRANCHANT

Department of Animal and Poultry Science, University of Guelph, 1Agriculture and Agri-Food Canada,
2
Department of Pathobiology, University of Guelph, Guelph and 3School of Food Science and Nutrition,
Université de Moncton, Moncton, New Brunswick, Canada

Abstract 1. Genetic parameters for the sudden death syndrome (SDS) were estimated in meat-type
chickens. Data were collected over 11 generations of selection for body weight within two distinct
breeds (Cornish and White Rock).
2. The animal model was used exclusively with linear methods (LM) to estimate genetic parameters.
Heritability (h2) of SDS on the liability scale was 0.30
0.002 and 0.25
0.002 in the Cornish and White
Rock breeds, respectively.
3. A positive genetic correlation (rg) with ascites (AS) was determined (0.3
0.006). However, it was
not possible to estimate the rg of SDS with body weight because of the low prevalence of the defect
trait studied (1.8% in the Cornish and 1.5% in the White Rock).
4. Heritability of SDS calculated using male records only was 0.45
0.009 and 0.35
0.009, and rg with
body weight was 0.30
0.010 and 0.27
0.009, in the Cornish and White Rock breeds, respectively.
5. In conclusion, the heart defect investigated was heritable with a positive genetic correlation with
AS and body weight.

INTRODUCTION of SDS increased appreciably as the flock body

Sudden death syndrome (SDS), also known as
‘flip-over’ or ‘acute death syndrome’, is a disease
of young and fast-growing broiler chickens which
die suddenly and occasionally on their back, with
about 60 to 80% of those affected being males
(Bowes et al., 1988). It has been suggested that
SDS is a metabolic disease causing ventricular
fibrillation, with the mortality peak ranging from
1 to 3 weeks of age, usually coinciding with the
age at which the rate of feed conversion is
greatest ( Julian, 1988). This topic has been fully
discussed by Olkowski and Classen (1995) and
Julian (1996).
A variety of factors such as nutrition, gene-
tics and environmental factors can affect the
incidence of SDS (Riddell, 1991), causing most
of the modern broiler chicken strains to be
susceptible. Different strains exhibit different
degrees of susceptibility to SDS (Riddell, 1993).
Gardiner et al. (1988) showed that the incidence
weight increased, an indicator of the existence
of a positive phenotypic correlation (rp) with
body weight, which leads to the possibility of
a high genetic correlation (rg). However, the
estimation of genetic parameters of SDS, includ-
ing heritability (h2), has been difficult to imple-
ment. These difficulties are attributable in part to
the relatively low prevalence of this disorder and
to its threshold nature.
One approach for estimating the genetic
parameters for threshold traits is linear methods
(LM). An attractive feature of LM is that the
animal effect can be readily incorporated into the
model. Although, according to Gianola (1982)
and Höschele (1986), LM predictions may not
be free of bias because of the non-additivity
present in the observed scale, other studies
have demonstrated little practical difference
between them and those estimated using non-
linear methods (Schaeffer and Wilton, 1976;
Berger and Freeman, 1978; Thompson et al.,

Correspondence to: Dr H.K. Moghadam, Department of Zoology, University of Guelph, Guelph, Ontario, Canada N1G 2W1. Tel: þ1-519-824-4120 ext
8596. E-mail: hkhalegh@uoguelph.ca
Accepted for publication 9th September 2004.

ISSN 0007–1668(print)/ISSN 1466–1799(online) ß 2005 British Poultry Science Ltd

DOI: 10.1080/00071660400023862
 GENETICS OF SUDDEN DEATH SYNDROME
1981; Boettcher et al., 1998), even when the
incidence of one category is low (Mercer and
Hill, 1984; Moghadam et al., 2001).
Moghadam et al. (2001) have previously
reported h2 estimates for ascites (AS) in broilers.
Using the same data-set, the objectives of the
present study were to estimate the h2 of SDS on
the liability scale and its genetic correlation with
AS and body weight in two breeds of meat-type
chickens, namely, Cornish and White Rock.
MATERIALS AND METHODS
Data collection
55
cavity. These chickens had usually died by 105 d
of age.
Statistical analyses
Genetic estimations were based on the analyses
of binary data in the LM. The PEST software
(Groeneveld and Kovac, 1990) was used to
re-code edited data. The restricted maximum
likelihood (REML) method was then applied to
estimate rg and h2 on the observed scale by using
the VCE4 software (Groeneveld, 1998). Both
two- and three-trait animal models (AM) with the
following general equation were considered:
Data were obtained from broiler strains of
chickens reared between 1981 and 1992 at the
Animal Research Center, Agriculture Canada,
Ottawa, Canada. Cornish (sire population) and
White Rock (dam population) breeds were
Y ¼ X þ Zu þ e
where Y is the vector of observations, X is the
incidence matrix for the fixed effects (sex, strain,
generation), Z is the incidence matrix of random
evaluated during one generation of random
mating and 11 generations of selection. Progeny
were obtained from parents that were randomly
mated with the exclusion of either full or half-sib
mating.
In the first 5 generations, the sire population
consisted of an unselected strain (control)
and three selected strains with two replicates.
In the initial generation, parents were selected
at random, whereas in subsequent generations
all the strains were selected for high 28-d
body weight. The dam population also consisted
of a control strain and a selected strain with
two replicates. In generation 5, the parents from
the selected replicate strains (in both sire and
dam populations) were crossed to combine
the replicate strains selected for the same trait.
Subsequently only one strain was kept for each
programme of selection. Additional details
can be found in the papers by Chambers et al.
(1984), Wang et al. (1991) and Moghadam et al.
(2001).
Dead chickens were necropsied and a diag-
nosis assigned. Those with evidence of heart
failure were classified as either acute or chronic.
Those with acute heart failure were classified as
cases of SDS (or ‘flip-over’ disease). Symptoms
leading to this diagnosis included: contracted
heart muscle; ruptured heart tissue; heart attack
(but not congested); ‘flip-over’ attached to report
from the barn (chicken found dead lying on its
back); heart tissues appeared healthy. These
chickens had died by 65 d of age. Chickens that
died of chronic heart failure were classified
as cases of AS (pulmonary hypertension, right
ventricular failure). Symptoms leading to this
diagnosis included: congestive heart failure;
enlarged right ventricle; heart tissues were
often turgid or flaccid; heart was not constricted;
ascetic fluid accumulated in the peritoneal
effects (animal),  is the vector of unknown
parameters for fixed effects, and u is the vector of
unknown parameters for random effects. Values
of h2 estimated on the observed scale were
transformed to the values on the liability scale
by using the following equation:
h2o ðð pð1  pÞÞ
h2l ¼
z2
where h2l is the estimation of h2 on the liability
scale, h2o is the h2 on the observed scale, p is the
proportion of affected individuals, and z is the
height (in standard deviation units) of the normal
curve at the threshold point and is equal to i  p,
where i is the mean deviation from the popula-
tion mean of animals with values exceeding the
threshold (Falconer, 1965).
RESULTS AND DISCUSSION
Phenotypic variance was calculated from a
binomial function of the prevalence. The pre-
valence of the defect trait in both populations
was relatively low, ranging from 1.5 to 1.8%
(Table 1) in the White Rock and Cornish breeds,
respectively. A three-trait animal model was used
to minimise the bias attributable to the effects of
selection on 28-d body weight. Many of the
elements in the right-hand side of the mixed
model equations were either 1 or 0. Because the
numbers of sires, dams, and progeny tested per
strain were relatively large, a high accuracy was
expected.
Difficulties were encountered in trying to
estimate the genetic correlations of SDS with
body weight. This was probably attributable to a
combination of (i) low incidence of the ailment
studied and (ii) missing values of body weight
56 H.K. MOGHADAM ET AL.

Table 1. Distribution of sudden death syndrome (SDS) cases diagnosed within sire families
in the sire and dam populations
Total Total Number of sire families with one or more (up to 5) affected progeny
number of number of
individuals sire families
5 4 3 2 1

Cornish 41 586 2026 5 6 25 101 411

White Rock 21 505 1201 1 2 13 40 185

for diseased birds that died prior to weighing.
This reduction of the data available for analysis
probably contributed to the decreased reliability
of the results and hence the high standard errors.
Estimates of h2, after transformation from
the observed to the liability scale, genetic cor-
relations with AS, and the highlights of the
differential incidence of SDS across families for
the two populations, are presented (Tables 1
and 2). As illustrated, SDS was mostly restricted
to certain families; therefore, the relatively high
h2 and the similarity in the breeding values of
relatives were to be expected. This suggests that
the family selection strategy may be an effective
tool for reducing SDS in broiler flocks. The
values of h2 for SDS on the liability scale were
0.25 and 0.30 for the White Rock and Cornish
breeds, respectively. These values indicate that
despite the relatively low incidence of SDS,
additive gene action plays an important role in
determining susceptibility to the disease.
Chambers (1986) estimated the h2 of SDS for
the same two populations, considering one
generation. The heritabilities he estimated, after
transforming estimates to the liability scale, were
0.12 and 0.17 in the White Rock and Cornish
breeds, lower than the estimates found in the
present study. Higher estimates are probably
because of (i) inclusion of the animal effect into
the model and (ii) a much higher number of
experimental units (chickens), by considering
11 generations instead of one.
The positive and moderate genetic correla-
tions between SDS and AS (about 30%) may be
a favourable factor for lowering the incidence
of both defects simultaneously. Considering
both abnormalities together as a single trait
would obviate the need for detailed recording
of separate abnormalities and enable greater
selection pressure to be applied. However, by
considering them as a single trait, a lower h2
is to be anticipated, which is attributable to the
relatively low genetic correlation between the
traits.
Because of the higher prevalence of both
SDS and AS in males, the h2 estimated from
both sexes was expected to be lower than that
estimated using male records only (Table 3).
Both defects had a positive and moderate genetic
Table 2. Estimation of genetic parameters for sudden
death syndrome (SDS) and ascites (AS) in Cornish and
White Rock breeds1 using data from both sexes
Breed SDS AS
Cornish SDS 0.30
0.002 0.30
0.005
AS — 0.22
0.009
White Rock SDS 0.25
0.002 0.28
0.007
AS — 0.12
0.017
1
Estimated values of h2 (liability scale) on diagonals, and genetic cor-
relations off-diagonal.
correlation with body weight, ranging from 0.22
to 0.35. However, the phenotypic correlations
between these two traits were close to zero
(Table 3). The systematic difference between
genetic and phenotypic correlations may be
attributable in part to the nature of the 0—1
scoring of the dependent variable. It is also
possible that there were some negative environ-
mental correlations between the defect traits and
live body weight.
The above observations may have important
implications in terms of breeding practices. First,
the defect traits investigated had a moderate-
to-high component of genetic variation, of the
order of 10 to 40%. Therefore, due to the
relatively high values of h2, selecting against
both diseases may help reduce their occurrence.
Because both defects were limited to certain
families, family selection may be a useful strategy
to apply. Broadly speaking, in defining a selec-
tion strategy against a disease (or threshold trait),
low incidence is expected to result in low
selection intensity with the proportion of animals
selected having little influence on the selection
differential. However, different approaches
have been suggested to overcome this problem
(Falconer and Mackay, 1996). These can be
summarised as: (i) selection based on the mean
liability of a family rather than an individual;
(ii) selection based on the estimated breeding
values; and (iii) selecting for a genetically related
continuous trait. For example, one possibility
might be selection from those families with larger
ratios of heart weight to live body weight. As
shown by Havenstein et al. (1994), these ratios for
modern broilers decreased from 0.56% (in males)
and 0.51% (in females) in 1957 to 0.51% and
0.48% in 1991. Because relative heart size does
 GENETICS OF SUDDEN DEATH SYNDROME 57

Table 3. Estimations of genetic parameters for sudden death syndrome (SDS), ascites (AS) and body weight
(BW) in Cornish and White Rock breeds using male records only1
Breed SDS AS BW2 BW
(rg)3 (rp)4

Cornish SDS 0.45
0.009 0.35
0.070 0.30
0.010 0.010

AS — 0.41
0.009 0.22
0.010 0.015
BW — — 0.45
0.009 —
White SDS 0.35
0.009 0.33
0.010 0.27
0.009 0.030
Rock AS — 0.22
0.017 0.35
0.007 0.017
BW — — 0.30
0.002 —
1
Estimated values of h2 (liability scale) on diagonals, and genetic and phenotypic correlations off-diagonal.
2
BW ¼ body weight at d 28.
3
rg ¼ genetic correlation.
4
rp ¼ phenotypic correlation.

not change substantially with age (Havenstein
et al., 1994), this may be used as a criterion for
family selection.
The positive genetic correlation between
SDS and AS may make it possible to reduce
their incidence by selecting against one of them
or to consider them both as a single trait.
The defects also had an unfavourable positive
(moderate) genetic correlation with live weight.
Problems remain, however, because SDS and AS
are positively correlated with live weight, mean-
ing that selection programmes for body weight
are likely to increase, or at best maintain, the
current incidence of these abnormalities.
ACKNOWLEDGEMENTS
This research was supported by Poultry Industry
Council and Ontario Ministry of Agriculture
Research grants. The authors are grateful for
helpful comments provided by Dr Vincent
Ducrocq and the anonymous reviewer.
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