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Revue Méd. Vét., 2011, 162, 6, 279-283
Introduction
Deep pectoral myopathy (DPM), also known as Oregon
muscle disease or green muscle disease, was first described
in 1968 as “degenerative myopathy” in turkeys [6]. Subsequently
it was studied at the Oregon State University by Harper [10]
and his collaborators [17]. The disease involves the wing ele-
vating muscle known as the deep pectoral muscle or M.
supracoracoidus hence; it is referred to as degenerative myo-
pathy of the supracoracoideus (DMS).
A probable analogy can be drawn between this disease of
poultry and the so-called “march gangrene” (anterior tibial
syndrome) in humans [16]. The “march gangrene”, so-named
because of its occurrence among the military personnel, is an
ischemic necrosis of the muscle in the myofascial compart-
ment on the anterior of human tibia following increased
intra-compartmental pressure, clinically characterized by
swelling, redness and pain, paralysis of the extensor digito-
rum brevis, and loss of sensation in the first interdigital cleft.
This disease is not preceded by vascular disease or trauma,
but it is usually associated with a recent period of locomotor
activity in otherwise healthy individuals [19]. The muscle is
firstly swollen, pallid and oedematous, and in untreated cases
this condition progresses to necrosis which has been described
as appearing greyish brown and wood-hard [19]. The general
reaction of the muscle is that occurring in ischemia and changes
similar to those in the broiler muscle supracoracoideus may
be seen [19].
Initial attempts to discover the cause of DPM were unsuc-
cessful. Cultured tissue from affected turkeys failed to show
evidence of bacterial or viral infection [9]. In addition, dietary
supplementation with vitamin E, methionine and selenium
also failed to reduce the incidence of DPM in turkeys [9, 19].
GRUNDER et al. [7] could not find any difference in DPM
incidence between groups of turkeys fed with corn or wheat
based rations. The cause of DPM appears to be not related to
nutrition disequilibrium or to a pathogen.
SUMMARY
The purpose of the study was to investigate the prevalence of DPM (deep
pectoral myopathy) in young broiler chickens according to their live weight
during slaughtering inspection. Chickens (Ross 308 and Cobb 500) reared
under intensive conditions and slaughtered on 7 weeks of age were allotted
in 2 flocks of 20 000 birds each, named flock A and flock B, according to
the ratio live weight / carcass weight (2.3/1.7 and 2.6/1.9, respectively).
During deboning of the breast muscles, samples showing gross lesions of
the m. supracoracoideus were collected and a conventional histology was
performed. The overall DPM prevalence (for the 2 flocks) was 0.51% and
the specific prevalence by flock was significantly higher in the flock B (P < 0.01).
The frequency of early DPM lesions characterized by an acute inflammatory
reaction (oedema, haemorrhages and infiltrate of macrophages and hetero-
phils) coupled to a severe muscle discoid necrosis was significantly higher
in the flock A (P < 0.05) whereas the proportion of older lesions in which
the affected muscle showing a typical green colour before being replaced by
fibrous or adipose tissue was dramatically increased in the heaviest chickens
(flock B) (P < 0.001). These results confirm the DPM occurrence in meat-
type growing birds even in young broilers (7 weeks old).
Keywords: Deep pectoral myopathy, broiler chickens,
Bulgaria, histology, acute inflammatory reaction, muscle
necrosis.
RÉSUMÉ
Myopathie du pectoral profond : prévalence chez les poulets de chair
âgés de 7 semaines en Bulgarie
Le but de cette étude a été de déterminer la prévalence de la myopathie du
pectoral profond (MPP) chez de jeunes poulets de chair en fonction de leur
poids vif durant l’inspection des carcasses à l’abattoir. Des poulets (Ross
308 et Cobb 500) élevés en mode intensif et abattus à 7 semaines ont été
répartis en 2 groupes de 20000 oiseaux chacun, groupe A et groupe B, en
fonction du rapport poids vif / poids de la carcasse (respectivement 2,3/1,7
et 2,6/1,9). Durant le désossage des filets, les échantillons présentant des
lésions macroscopiques du m. supracoracoideus ont été collectés et analysés
par histologie conventionnelle. La prévalence globale de la MPP (pour les 2
groupes) a été de 0,51 % et la prévalence spécifique par groupe a été signi-
ficativement plus importante dans le groupe B (P < 0.01). La fréquence des
lésions précoces caractérisées par une réaction inflammatoire aiguë
(œdème, hémorragies, infiltrat par des macrophages et des hétérophiles)
couplée à une nécrose discoïde sévère du muscle a été significativement plus
élevée dans le groupe A (P < 0.05) alors que les lésions plus anciennes (dans
lesquelles le muscle atteint présente une coloration verte typique avant d’être
remplacé par du tissu fibreux ou adipeux) se sont avérées beaucoup plus fré-
quentes dans le groupe B, celui des poulets les plus lourds. Ces résultats
confirment l’existence de MPP chez les oiseaux sélectionnées pour la pro-
duction de viande, y compris chez des poulets jeunes (de 7 semaines).
Mots clés : Myopathie du pectoral profond, poulet de
chair, Bulgarie, histologie, réaction inflammatoire aiguë,
nécrose musculaire.
Deep pectoral myopathy: prevalence in 7
weeks old broiler chickens in Bulgaria
I. DINEV1*, D. KANAKOV2*
1Department of General and Clinical Pathology, Faculty of Veterinary Medicine, Trakia University, 6 000 Stara Zagora, BULGARIA.
2Department of Internal Medicine, Faculty of Veterinary Medicine, Trakia University, 6 000 Stara Zagora, BULGARIA.
*Corresponding author: idinev@uni-sz.bg
Revue Méd. Vét., 2011, 162, 6, 279-283
280 DINEV (I.) AND KANAKOV (D.)
It is generally recognized that DPM is an ischemic necrosis
that develops in the deep pectoral muscle (supracoracoideus
or pectoralis minor muscle) mainly because this muscle is
surrounded by inelastic fascia and the sternum, which do not
allow the muscle mass to shell in response to the physiological
changes occurring when muscles exercised, as in wing flap-
ping [12]. The lesion does not impair the general health in
birds and it is generally found during cut-up and deboning.
No public health significant problem is associated to DPM,
but it is aesthetically undesirable. The fillet should be removed,
whereas the rest of the carcass is still fit for human consumption
[12]. However, the required trimming operations determine
the downgrading of the products and produce an economic
loss for the industry, especially because it affects the more
valuable part of the carcass. Although this disease was first
recognized in adult meat-type turkey and chicken breeders, it
is becoming more and more common in meat-type growing
birds [3, 8, 13]. According to SILLER [17], DPM occurs
exclusively in birds that have been specially selected for
breast muscle development.
The purpose of the study was to present the results obtained
from slaughtering inspection and histopathology in sponta-
neous cases of deep pectoral myopathy (DPM) reported for
the first time in broiler chickens in Bulgaria, according to the
age and live weight of the birds.
Materials and Methods
ANIMALS
The investigation was carried out using the material from
a large Bulgarian poultry slaughterhouse in Stara Zagora.
Chickens were originated from a farm in the same province
where they were reared under intensive conditions and were
slaughtered on 7 weeks of age. The samples showing gross
lesions were collected during the deboning of breast muscles
of broiler chickens. The statistical analysis and comparison
of the incidence of the lesions were made during inspection
of carcasses originating from two different flocks (10 000
carcasses were inspected for each flock). The flocks consisted
of 20 000 birds each, belonging to both sexes and to 2 com-
mercial strains: Ross 308 and Cobb 500, mixed dispropor-
tionately. The mean life weight to mean carcass weight ratios
were 2.3/1.7 and 2.6/1.9 in the flock A and the flock B,
respectively.
HISTOLOGICAL ANALYSIS
After macroscopic examination, 10 samples with lesions
from the m. supracoracoideus were taken from each flock
for histological investigations. The samples were fixed in
10% neutral formalin, processed routinely and embedded in
paraffin. The obtained sections approximately 5µm were
stained with haematoxylin-eosin.
STATISTICAL ANALYSIS
The data were statistically processed by a chi 2 test for
comparing the 2 flocks. Differences were considered as
significant when P < 0.05.
Results
Table I shows the incidence and distribution of the DPM
characteristic lesions for both flocks, determined on the pro-
cessing line after the breast-deboning area. The overall inci-
dence of DPM was 0.51%. The total lesions incidence was
significantly higher in the flock B with the highest live/carcass
weight ratio than in the flock A (P < 0.01). The prevalence
of early lesions was twice higher in flock “A” (the birds with
lower live/carcass weight ratio) (P < 0.05) whereas later
stage lesions occurred much more frequently (≈10 times) in
heavier birds (flock “B”) (P < 0.001).
Macroscopically, early lesions showed oedema, hyperaemia
and haemorrhages of the supracoracoid muscle. One or both
supracoracoid muscles were affected at a various extent. The
changes vary by intensity from separate, focal to diffuse
damage affecting the whole muscle. Commonly the lesion
was sharply confined from the unaffected part of the muscle
(figure 1). The fascia overlying and separating it from the
superficial pectoral muscle was thickened, opaque and some-
times covered by a gelatinous matter. In older cases, the
acute oedema has disappeared. The affected muscles were
intensive green in contrast to the unaffected tissue and exhi-
bited single or multiple haemorrhages (figure 2). The green
areas were generally confined to the surface but gradually
they penetrated more deeply into the necrotic tissue leading
to the occurrence of irregular green bands of varying thickness
surrounding the pale necrotic muscle in cross section. In the
oldest lesions, the colour intensity of the muscle was alleviated,
1Flocks were characterized by the ratio mean live weight / mean carcass weight;
Different superscripts a,b in the same column indicate significant differences between flocks (P < 0.05) with a chi 2 test.
Flocks1Early lesions Older lesions Total lesions
Flock A (2.3/1.7)10.32%a0.05%b0.37%b
Flock B (2.6/1.9)10.16%b0.48%a0.64%a
Total 0.24% 0.27% 0.51%
TABLE I: Incidence of DPM (Deep pectoral myopathy) in the 2 flocks of broiler chickens reared under intensive conditions in the farm
in Stara Zagora province.
Revue Méd. Vét., 2011, 162, 6, 279-283
PREVALENCE OF DPM IN BROILER CHICKENS 281
becoming pale yellow-green, and haemorrhages were reduced
(figure 3). The necrotic muscle bundles appeared dry and
brittle and usually the entire lesion was enclosed by a thick
connective tissue capsule sequestrating it from the remaining
muscle tissue. Sometimes the affected muscle appeared with
reduced volume, fibrous and hard.
The histological investigations confirmed the acute inflam-
mation in early DPM lesions. Degenerative necrotic changes
or sometimes Zenker’s degeneration, increased acidophilia
and oedema were observed. An infiltrate of inflammatory
cells (mainly macrophages and some heterophil leukocytes)
was found in the affected area (figure 4). The necrosis of the
muscle bundle was arranged as a discoid form and the so-called
discoid necrosis resulted in the separation of the individual
sarcomeres (figure 5). In the more chronic lesions, the muscle
fibres were almost entirely replaced by fibrous and/or adipose
tissue (figure 6).
Discussion
In the present study, the DPM prevalence is significantly
more elevated in the heavier chickens. This finding is in
agreement with CRESPO and SHIVARPRASAD [5], sug-
gesting that DPM is mostly prevalent in heavy birds.
Moreover, as in the present study, the incidence of old
lesions, indicating the chronicity of the muscle degeneration,
was markedly higher in the biggest chickens, the DPM can
FIGURE 1: Above – early lesion of DPM (Deep pectoral myopathy) cha-
racterized by oedema, hyperaemia and discoloration of the m.
supracoracoideus. The lesion is sharply delineated (arrow) from
the unaffected part. Below – normal m. supracoracoideus.
FIGURE 2: Old lesion of DPM (Deep pectoral myopathy). The affected
muscles are intensive green (G) in contrast to the unaffected tissue
and with multiple haemorrhages (H).
FIGURE 3: Older DPM (Deep pectoral myopathy) lesion, with pale yel-
low-green colour and reduction of the haemorrhages in the affected
muscle.
FIGURE 4: Degenerative necrotic changes (Zenker’s degeneration) (zd),
increased acidophilia (a), heterophil leukocytes (h) and macrophages
(m) among dead muscle tissue, Haematoxylin-eosin, bar: 35 μm.
Revue Méd. Vét., 2011, 162, 6, 279-283
282 DINEV (I.) AND KANAKOV (D.)
be associated with the tendency to produce “heavy” broilers
(> 3kg live weight) for breast muscle [1]. Some authors [1-4,
8] have evaluated the incidence of the muscular disease in
heavy male roaster chickens reared in commercial condi-
tions. However, it is difficult to compare these results with
the current study where chickens were both males and females.
Nevertheless, DPM cases in the present study were observed
in young birds (7 weeks old) and this age was previously
reported by RICHARDSON et al. [13] as the lowest for evi-
dencing such muscular lesions. The mean live/carcass weight
ratios of the chickens with DPM lesions are among the
lowest ever reported [13]. These facts support the concept
that the DPM prevalence is higher in meat-type growing
birds [3, 8, 13] and according to SILLER [17], DPM occurs
exclusively in birds that have been specially selected for
breast muscle development, as the 2 commercial strains
(Ross 308 and Cobb 500) used in this assay. Evidence that
this condition only appears because of intensive selection is
supported by the absence of DPM in wild turkeys, even when
these birds are experimentally forced to grow [2, 4, 17].
The DPM lesions firstly exhibited an acute inflammatory
aspect with oedema, hyperaemia and haemorrhages of the
supracoracoid muscle. The lesions can be focal or diffuse,
affecting the whole muscle and can be spread to the both
supracoracoid muscles. However, the uni- to bilateral lesion
ratio was not determined in the present study. The acute
inflammation reaction was histologically confirmed by oedema
and cell necrosis and the presence of an inflammatory infiltrate
constituted mainly with macrophages and some heterophils
was noted in injuried muscles. Furthermore, lot of muscle
fibres appeared as markedly necrotic (Zenker’s degenera-
tion) and the discoid necrosis lead to the destruction of the
muscle architecture. Older lesions were mainly characterized
by a marked green colour of the affected muscles. By analogy
with bile pigments it was firstly assumed that this green colo-
ration derived from the degradation of a haemic pigment,
such as haemoglobin or myoglobin, during the development
of myopathy [15]. The resistance to acidic solvents shows
that the pigment was covalently bound to protein [14] and in
1978, SILLER and WINGHT [15] suggested that this pig-
mentation may be due to the accumulation of one cytochrome,
probably the cytochrome b. Thereafter, this pigmentation
gradually disappeared in lesions evolving for a long time
characterised by a chronic inflammation, leading to the muscle
fibrosis and to the formation of a fibrous capsule in periphery
[15]. Histologically, the muscle tissue gradually disappeared
and was substituted with fibrous then adipose tissues, the
connective tissue reaction usually beginning from the intact
tendon [18].
There is a genetic predisposition of large-breasted birds to
this muscular disease. Possible aetiology explanation for this
disease may be related to an inadequate vasculature in meat-
type birds [17]. Some evidence has been produced for a here-
ditary susceptibility of DPM [11]. The selection of these
breeds would be associated with a gene mutation leading to
apoptosis of myocytes frequently coupled to cytochrome
accumulation in cytoplasm and inherent caspase activation
or leading directly to the accumulation of the haemic proteins
which in turn provoke the caspase cascade. Moreover, this
data suggests that genetics may play an important role in the
determination of DMP.
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