THE GREEN MUSCLE DISEASE IN

CHICKENS AND TURKEYS

A. A. Grunder

Animal Research Centre, Agriculture Canada,

Ottawa, Ontario, Canada KIA 0C6

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THE GREEN MUSCLE DISEASE IN

CHICKENS AND TURKEYS

A.A. Grunder

Animal Research Centre, Agriculture Canada,

Ottawa, Ontario, Canada KIA 0C6

1. Introduction.

Green muscle disease was first reported by Dickinson et al. (1968) in

turkeys and later in meat-type chickens by Harper et al. (1971). The disease

involves the wing elevating muscle known as the deep pectoral muscle or the

M. supracoracoideus; hence, it is referred to as degenerative myopathy of the

supracoracoideus (DMS). Generally the disease is found in mature and often

spent breeders but has been observed in seven-week-old broiler chickens byRichardson et al. (1980).

Early stages of the disease are characterized by edema and hemorrhage of

the supracoracoideus. There may be a greenish color evident at this time.

Later, one or more encapsulated areas of green fibrous tissue will appear and

thus the name green muscle disease. Later stages are characterized by varying

degrees of atrophy of the muscle and partial replacement by fibrous and fatty

tissue. One or both supracoracoidei may be affected to varying degrees. Thedisease has been likened to "march gangrene" (anterior tlbial syndrome) of man

(Siller et al., 1979a).

2. Cause of the disease and its pathogenesis.

Initial attempts to discover the cause of DMS were unsuccessful. Cultured

tissue from affected turkeys failed to show evidence of bacterial or viral

infection (Harper and Helfer, 1972). These same investigators failed to alter

incidence of DMS in turkeys by giving added vitamin E, methionine and selenium

to the ration. Grunder et al. (1979) could not find any difference in DMS

incidence between groups of turkeys fed either corn or wheat based rations.

The cause of DMS was not related to nutrition or a pathogen.

To elucidate the cause of the disease, scientists in Edinburgh focused on

the M. supracoracoideus. Pathological investigations revealed that DMS is dueto ischaemlc (lack of blood) necrosis of the muscle whether in turkeys (Siller

and Wight, 1978) or broiler breeder hens (Wight and Siller, 1980). They were

able to produce the disease experimentally in a strain of light-weight layinghens by occluding the subclavian artery (Siller e_tt a_ll., 1978) and in broilerbreeder hens by electrical stimulation of the muscle, either directly or viathe pectoral nerve (Wight et al., 1979). Such muscle stimulation caused

necrosis; hence, the Edinburgh scientists thought that voluntary activity of

the muscle, such as flapping the wings, could cause the disease. ThereforeSiller et al. (1979b) induced birds to flap their wings until exhausted and

produced acute DMS in 73% of caged and 40% of penned broiler breeder hens, all

of the 5 adult turkeys exercised but none of the 6 adult egg-type fowls. The

investigators hypothesized that muscle fascia prevented muscle enlargement of

exercised birds with a resultant lack of blood supply. They tested the

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hypothesis by surgically cutting the fascia of a number of birds and then

stimulated the muscle by electrical stimulatlon of the pectoral nerve or by

induced wing-exercise. Prevention of DMS was achieved regardless of type of

muscle stimulation (Siller et at., 1979a). Thus they had an explanation for

the pathology of the disease and a method of inducing it.

3. Indirect methods for detecting DMS.

Aside from performing autopsies, DMS may be detected in live turkeys and

dressed turkeys by means of palpating and observing sunken areas on the breast

(Harper et al., 1975). It was assumed that such sunken areas are present only

after considerable atrophy has taken place because early stages of DMS cannotbe observed on the live turkey. I have not been able to detect advanced cases

of DMS in live chickens by palpation. A method for detecting affected turkey

carcasses was developed by Jones (1977) without exposing the

M. supracoracoideus. He used a light-probe which, when inserted into the body

cavity, revealed abnormal images near the keel bone if DMS were present. This

method removes the necessity of cutting open breasts, including those of

normal turkeys, for detection and thereby lowering the value of the carcass.

Use of the plasma enzyme creatine kinase (CK) as a means of detecting DMS

in turkeys was investigated by Hollands et al. (1980). Measurement of thi_

enzyme's activity is one of the diagnostic tools used in clinical medicine for

detecting myocardial necrosis. Plasma CK values were measured in 70 female

Small White turkeys by blood sampling each bird 18 to 20 times over an age

span of 16 to 79 weeks. Autopsy of all birds revealed a 15.7% incidence. Of

the affected birds, 82_ had a CK value which deviated three or more standard

deviations from the mean of all values for the same bird. Using this

criterion for rejections of birds in a selectlon experiment, 82% of the birds

would have been rejected correctly and 5% would have been rejected incorrectly(Table 1).

With the knowledge provided by Siller and his colleagues that induced wing

exercise would cause DMS, Hollands et al. (1981) exercised 14 turkeys, bled

them at various times post-exercise to determine plasma CK activity and then

killed the birds for DMS diagnosis. As Fig. 1 shows, maximum difference

between the means of CK values of the 6 affected and 8 normal turkeys occurred

3 days post-exercise. There was no overlap in range of values between

affected and non-affected birds from day 2 to day 8 post-exercise. This

method showed great promise for selecting non-affected birds for a breedingprogram. - .......

A larger experiment of this same kind was conducted using year-old broilerchicken populations. A stock from each of two commercial companies wasrepresented and will be referred to as a genetic base. The 19-20 birds ofeach sex of the two bases (coded E and F) were bled, wing exercised twice withan hour between each effort, then bled at various intervals up to 17 times andkilled 22 days after exercise. Each bird was classified for DMS as either

negative, chronically affected before exercise, or acutely affected afterexercise. The means ± standard deviations of plasma CK levels before exerciseand 1, 2, 6 and 22 days post-exercise are shown in Table 2. Peak values wereobtained one day after exercise for all stock and sex combinations of each

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autopsy classification. Although mean CK values of each class were wellseparated by one day post-exercise and ranked acute, chronic and negative(high to low), ranges (not shown) generally overlapped except for acutelyaffected and negative birds of Base E which normally exhibits a higher DMSincidence than Base F.

A much larger investigation of post-exercise induced DMS and plasma CK wasconducted on the third selected generation of high and low DMS incidencestrains and a non-selected control strain derived from commercial broiler

chicken bases E and F. Details of the selection procedures will be describedlater. At 19 or 20 weeks of age chickens were exercised, bled one, two or

three days later and plasma CK was assayed. All birds were killed and

autopsied 9 or 16 days post-exercise and classified positive (acutely and/or

chronically affected) or negative. As shown in Table 3, there were

significant differences in CK values between affected and non-affected birds,

between sexes, among strains but not between bases. As with the year-old

chickens, the peak mean plasma CK values occurred one day post-exercise. Thiswas also the time of maximum difference between affected and non-affected

birds.

As with the year-old chickens, ranges of CK values for the 19-20 week oldbirds overlapped for affected and non-affected birds even on day one

post-exercise and thus differentiation on the basis of CK cannot be perfect.

Frequency plots of affected and non-affected males and females with classintervals of 20,000 international units per liter, were prepared on data

collected one day post-exercise. There was a skewness to the left where most

of the non-affected birds were plotted but there appeared to be a slight

valley where this skewed population on the left met the tailed population on

the right (Fig. 2 and 3). If one drew a line parellel to the ordinate at this

meeting point for males and all birds to the left were saved for future

breeding, then 66% of the non-affected and 14% of the affected birds would be

saved. Likewise, if the same procedure were repeated for females, then 60% of

non-affected and 1% of affected would be saved. Although not 100% efficient,

selection on the basis of induced high values of plasma CK should be fairly

effective in selecting birds comparatively resistant to DHS for use in

breeding populations.

4. Genetics of Green Muscle Disease.

The first observations made on the heredity of this disease were made in

turkeys by Harper et al. (1975). They reported that data from a processing

plant showed a greater incidence of DHS in white turkeys than in BroadBreasted Bronze turkeys. During a selection study over seven years they were

able to increase the incidence, decrease the age of occurrence and decrease

the differential incidence between sexes, females having a higher incidence

than males. They concluded that DHS is variable in expresslvity and

penetrance and is apparently under the control of a polygenic system involvingmodifiers.

4.1 Strain differences in DMS incidence.

Interest in the incidence and genetics of DHS in meat-type chickens in my

laboratory occurred when Hollands et al. (1981) surveyed several stocks for

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DMS (Table 4). Cor_nercial stocks E and F on a nutrition experiment eachcomprised male and female parents and together were considered as 4 geneticstocks. There were also 9 male parent stocks and 7 female parent stocksbrought into Ottawa in 1978 from commercial primary breeders for the purposeof synthesizing populations to be used in a selection study to reduce broilerfatness. There were also three experimental strains synthesized fromcon_uercial broiler stocks in 1958 and represented broiler stocks from an

earlier period (Chambers et al., 1981). For the 6 groupings of commercialstocks as shown in Table 4, chi-square values were significant in 5 of 6analyses indicating that within the groupings, the various commercial

meat-type stocks differed in DMS incidence. The nine possible sex comparisonsin Table 4 resulted in only two significant chi-squares. Therefore incidencein the two sexes is comparable. In contrast, no DMS was found in the femalesof experimental stocks representing commercial strains of 15 to 20 years ago.Therefore, DM$ incidence seems to be associated with the more rapid growth andheavier adult weight of the modern broiler. In any case, the data suggest

that genetic differences exist between commercial broiler strains with respectto susceptibility to DMS.

4.2 DMS and production traits.

The association between DMS and economic traits was tested using data ofthe 9 male and 7 female parent stocks listed in Table 4. The average 365-daybody weight of the DMS-positive females was 154 g higher than the average ofthe remaining birds (3748 g v s 3594 g; P < .01). For all surviving males andfemales measured at 42 days of age, the breast angle of birds that developedDMS lesions was 4 degrees greater than in the negative birds (93 v__ss89degrees; P < .05). In all other traits analyzed there were no significanteffects associated with DMS. The evidence suggests that DMS increased as aresult of selection for growth rate and meatiness of breast as reflected inbreast angle.

4.3 Selection for DMS incidence.

A selection experiment was initiated in broiler chicken stocks with theobjective of changing the incidence of DMS. Male and female parents from eachof commercial stocks E and F were mated, 50 males x 100 females to produce arandombred pedigreed population. Based on DMS incidence in parents of the

randombred populations, for each genetic base, matings were made up to producegeneration 1 of a high DMS incidence strain, low DMS incidence Strain and a_unselected control strain (Table 5). Fifteen males were mated to 30 femalesfor each of the selected strains and 30 males were mated to 60 females for the

control strain for this, and generations 2 and 3. Generation 2 was producedafter selecting parents based on exerclse-induced DMS of the randombredgeneration. Generation 3 was produced after selecting parents based on plasmaCK levels observed after generation 2 had been exercised at 18 weeks of age.Birds of Generation 3 were exercised at 19 or 20 weeks and killed at 21 weeks,classified for DMS and the selection experiment was terminated. In additionto incidence of DMS, economlcally important traits were measured.

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Response to selection for DMS is shown in Fig. 4 where incidences of DMSper generation of the high and low strains are plotted as deviations from thecontrol strain. Overall incidence of DMS in 2494 birds of generation 3 was

34, 20 and 18% for the high, control and low strains respectively. Withineach genetic base and sex, strain differences were significant (P < .01) in 3

of 4 comparisons.Inspection of Fig. 4 shows that in this short selection experiment,

selection response for the single trait DMS incidence was erratic.Essentially no progress was made in selecting for low DMS incidence in baseF. The reason may be the somewhat lower DMS incidence in stock F comparedwith stock E observed prior to the experiment, as recorded in Table 4.However, in base E, Fig. 4 indicates that progress was made in selecting forlow DMS incidence in generation 3.

Although generation 3 birds were killed at 21 weeks of age, thus

preventing the collection of egg production records, records of body weightand breast angle were analyzed. The summary of means shown in Table 6indicates that birds affected with DMS had greater (P < .001) 56-day body

weight, housing body weight and breast angle than non-affected birds. Thisassociation between DMS and heavy body weight and large breast angle isconsistent with the previously discussed association observed in the

commercial parent stocks brought to Ottawa in 1978. There were also

significant differences between bases and between sexes. The results of thisselection study suggest that continued selection for breast angle and bodyweight will result in ever increasing incidences of DMS unless there is

accompanying selection against this disease.Egg production traits were recorded for generations 1 and 2. Those of

generation 2 were considered most meaningful and a summary of means is shownin Table 7. There were no significant differences between affected andnon-affected hens for any of the egg traits except specific gravity. Base E

was slightly superior to Base F in egg production. There were no significantdifferences among strains for any of the production traits. Results of the

second generation of selection do not indicate that production traits wouldsuffer to any large degree by selecting in either direction for DM$ incidence.

Conclusions

1. Degenerative myopathy of the supracoracoid muscle is due to ischaemicnecrosis of this muscle because the fascia does not allow the muscle to

expand thereby resulting in stoppage of arterial blood flow. The diseaseoccurs mainly in adult turkeys and meat-type chickens.

2. The disease can be induced by wing exercise and presumably excessive wingexercise induces DMS in the field.

3. Detection of susceptibility to DMS in live birds by induced wing exerciseand measurement of plasma creatine kinase has potential as an aid toselection against DMS susceptibility in a breeding program.

4. Differences in incidence of DMS in both turkey and chicken stocks and the

response to selection suggest that predisposition or susceptibility isinherited and controlled by multiple genes.

5. Continued selection for growth rate and good body conformation will likelylead to increased incidence of DMS. Therefore selection against DMS

should be practiced.

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Table I. Rank of Ii female turkeys affected by DMS, of 70 birds total,

accordlnE to the maximum plasma creatine klnase (CK) value expressed

as units of standard deviation above the mean (18-20 blood samples

taken from each bird). Age of maximum plasma CK level is recorded

and CK levels were log e transformed and adjusted for bleeding dateeffects. (From Hollands, et al., 1980).

Bird Age Rank Standard deviations

(weeks) no.

A 54 1 6.72

B 58 2 5.82

C 51 3 4.62

D 60 4 4.31

E 47 5 4.05

F 32 6 3.81

G 49 7 3.68

H 54 11 3.33

I 52 12 3.24

J 60 17 2.71

K 20 29 1.94

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Table 2. Mean + standard deviation of plasma creatine klnase levels

(thousands of I.U. per liter) before exercise and 1, 2, 6 and 22

days post-exercise of chickens at 1 year of age and classified as

acute, chronic or negative for DMS

Autopsy Pre- __ Days Post-Exercise

Base Sex Classification No. Exercise 1 2 6 22

E Male Acute 2 10±9 232±41 170±6 47±18 4±1

Chronic 7 5±2 154±67 82±37 14±7 3±2

Negative 11 7±8 33±22 12±9 7±9 4±4

Female Acute ii 5±12 405i193 364±308 34±22 3i3

Chronic 4 2i3 239±114 164±108 7±3 li.2

Negative 4 li.5 37±25 16±13 2±2 3±4

F Male Acute 7 5±1 342+--165 193±103 45±34 4±12

Chronic 5 3±2 202+_95 114±68 18+-16 2±.3

Negative 8 12+--27 80±61 41±56 10±14 8±17

Female Acute 6 3±2 302±101 199±87 32±15 4±2

Chronic 7 1±1 179+_98 116±75 8±4 1±1

Negative 7 9±18 66±79 39±49 11±12 5±10

1Classified for DMS as follows: Acute = affected as the result of the

exercise and may include evidence of chronic DMS; Chronic = affected prior

to exercise; Negative = non-affected.2

22 Days post exercise no. = 4.

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Table 3. Least squares means and significance of differences in plasma

creatine kinase (thousands of I.U. per liter) of generation 3

chickens 1, 2 or 3 days post-exerclse at 19 or 20 weeks of age

Source of Total Days post-exerclse

variation No. 1 2 3

Autopsy class _ _ _*_

Affected 555 407 245 186

Non-affected 1137 128 66 38

Sex RR _R_ _R_

Male 751 237 106 95

Female 941 297 205 129

Base

E 895 257 152 111

F 797 278 159 113

Strain _- *. **_

Hish 423 304 186 142

Control 731 264 156 114

Low 538 234 126 80

_" P < .01; _* P < .001.

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Table 4. The incidence of DMS in 20 commerclal parent stocks and 3

experimental strains 1

Males FemalesStocks

No. % DMS No. % DMS------X2 for sex

Examined Examined differences

Commercial parent stocks, pen housing

E 26 31 205 21

F 92 17 213 11

X 2 = 2.2 X 2 = 8.8,_

Male parent commercial stocks, pen rearing, individual cage housing

11 32 3 79 19 4.7"21 31 19 74 22 .0731 35 1141 32 651 33 3

61 34 3 75 4 .0771 30 0

81 36 0 82 1 .4491 28 43

X 2 = 53** X 2 = 25,x

Female parent commercial stocks, pen rearing, individual cage housing

12 35 3 69 17 4.48 x22 39 18 71 13 .5632 36 6 71 7 .0942 69 3

62 32 0 64 3 1.02

72 68 O

82 28 0 74 12 3.73X 2 = 14" X 2 = 22**

Experimental Ottawa strains, pen rearing, individual cage housing

A 25 0D 25 O

Z 25 0

1 Stocks E and F were broiler parent stocks from two commercial breeders;within each stock, males and females belonged to a different primary strain

and thus E and F include 4 genetic groups. For the remaining commercialstocks, the first digit designates commercial breeder source, the second

digit type of stock: 1 = sire-type, 2 = dam-type. Males and females of

each commercial stock, were considered part of the same grand-parent stockfor a total of 16 genetic 6roups.

2 Sex differences in stocks E and F were not tested because males and

females were believed to be from different strains.

* F < .05.** P < .01.

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Table 5. Numbers of birds in a study of selection for DMS incidence in which

high (H) and low (L) incidence strains and a control (C) strain were

formed

Progen_ 1

Housed SelectedGeneration Base Strain M F M F Criterion

0 E ].03 275 56 120 Parental DMS

F 96 332 53 119 Parental DMS

1 E,F H. 55 113 15 30 Parental DMS

C 60 109 30 60 Random _

L 54 116 15 30 Parental DMS

2 E,F H 107 125 15 30 Creatine kinase

C 146 201 30 60 Random

L 88 115 15 30 Creatine kinase

32 E,F H 132 139

C 3OO 334

L 159 182

1For generations 1,2 and 3, numbers represent averages per base for each of

the H, C and L strains. See text for explanations of each selection

criterion.......

Chickens of generation3 were hatched-and reared to 21weeks of age but ....

not housed.

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Table 6. Least squares means and significance of differences in body weight

and breast angle after 3 generations of selection for DMS

Source of 56-day Housing Housing

variation body weight body weight breast angle

(dg) (dg) (°)

1Autopsy class "_ _ _

Affected 220.5 334.4 97.4

Non-affected 216.2 312.2 93.0

Sex R_R RRR _RR

Male 243.2 360.4 92.6

Female 193.5 286.2 97.8

Base _R_ _,R

E 218.9 329.5 94.2

F 217.8 317.1 96.2

Strain _

High 216.8 324.0 96.2

Control 220.0 326.2 95.7

Low 218.2 319.6 93.6

1Total birds were 565 affected and 1302 non-affected.

P < .05; _ P < .01; _ P < .001.

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Table 7. Least squares means and significance of differences in egg

production traits for survivors after 2 generations of selection for

DNS

........... 220 days

Age to Total eggs Age to Egg

Source of first egg first egg Eggweight specific Haugh

variation (days) to 322 days hen day % (g) gravity units

1Autopsy class

Affected 193.5 93.6 71.5 55.6 1.0894 88.0

Non-

affected 191.5 97.3 72.9 55.7 1.0878 88.7

Base • ,z R

E 190.4 99.2 74.1 55.2 1.0889 89.0

F 194.6 91.7 70.3 56.1 1.0883 87.7

Strain

Nigh 194.1 94.9 72.5 55.6 1.0885 88.6

Control 192.7 96.2 73.1 55.9 1.0881 88.6

Low 190.7 95.2 70.9 55.5 1.0892 87.8

1Total hens were 76 affected and 658 non-affected.

P < .05; _ P < .01.

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32x = DMS (n = 6)

30 - = Normal (n = 8)

28

26

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20

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Days post-exercise

Figure i. The effect of exercise on creatine kinase (CK) plasmalevels in turkey hens that were subsequently diagnosed DMS posi-tive or normal with the mean of the CK values and the range shown

for each bleeding time.

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Figure 4. Incidence of DMS for the high and low selected strains plotted

as deviations from incidence in the control strains. Numbers along the

0 lines represent percent incidence in the control strains.

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REFERENCES

Chambers, J.R., J.S Gavora and A. Fortin, 1981. Genetic changes in meat-typechickens in the last twenty years. Can. J. Anim. Sci. 61: 555-563.

Dickinson, E.M., J.O. Stevens and D.H. Helfer, 1968. A degenerative myopathyin turkeys. Proceedings of the 17th Western Poultry Disease Conference,

University of California, Davis, p. 7.Grunder, A.A., K.G. Hollands and J.S. Gavora, 1979. Incidence of degenerative

myopathy among turkeys fed corn or wheat based rations. Poultry Sci. 58:1321-1324.

Harper, J.A., D.H. Heifer and E.M. Dickinson, 1971. Hereditary myopathy inturkeys. Proceedings of the 20th Western Poultry Disease Conference,University of California, Davis, p. 76.

Harper, J.A. and D.H. Heifer, 1972. The effect of vitamin E, methionine andselenium on degenerative myopathy in turkeys. Poultry Sci. 51: 1757-1759.

Harper, J.A., P.E. Bernier, D.H. Heifer and J.A. Schmitz, 1975. Degenerativemyopathy of the deep pectoral muscle in the turkey. J. Hered. 66: 362-366.

Hollands, K.G., A.A. Grunder, C.J. Williams, J.S. Gavora, J.R. Chambers andN.A.G. Cave, 1981. Degenerative myopathy in meat-type poultry: its effect

on production traits in chickens and its identification in live turkeys.Quality of poultry meat in Proc. Fifth European Symposium. Apeldoorn, TheNetherlands. p. 337-344.

Hollands, K.G., A.A. Grunder, C.J. Williams and J.S. Gavora, 1980. Plasmacreatine kinase as an indicator of degenerative myopathy in live turkeys.

British Poultry Science 21: 161-169.Jones, J.M., 1977. Quick detection now for Oregon. Poultry Industry, July

1977. p. 14-15.Richardson, J.A., J. Burgener, R.W. Winterfield and A.S. Dhillon, 1980. Deep

pectoral myopathy in seven-week-old broiler chickens. Avian Dis. 24:1054-1059.

Siller, W.G. and P.A.L. Wight, 1978. The pathology of deep pectoral myopathy

in the turkey. Avian Pathology 7: 583-617.

Siller, W.G., L. Martindale and P.A.L. Wight, 1979a. The prevention of

experimental deep pectoral myopathy of the fowl by fasciotomy. Avian

Pathology 8: 301-307.

Siller, W.G., P.A.L. Wight and L. Martindale, 1979b. Exercised-lnduced deep

pectoral myopathy in broiler fowls and turkeys. Veterinary ScienceCommunications. 2: 331-336.

Wight, P.A.L., W.G. Siller, L. Martindale and J.H. Filshie, 1979. Theinduction by muscle stimulation of a deep pectoral myopathy in the fowl.Avian Pathology 8: 115-121.

Wight, P.A.L. and W.G. Siller, 1980. Pathology of deep pectoral myopathy of

broilers. Veterinary Pathology 17: 29-39.

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1983 NATIONAL BREEDERS' ROUNDTABLE

Questions to Dr. Allan Grunder Title: "The Green Muscle Disease inChickens and Turkeys"

Question from Kenneth Goodwin: What is the fate of the bird which contractsthis disease? Does it die?

Answer: The disease apparently does not cause any ill effects to the bird.The disease in itself does not cause death and affected birds seem to

live as long as non-affected birds.

Question from Ramakrishna Redd¥: What is the frequency of DMS in the broilerpopulations in your study? Is DMS important from the commercial stand-

point at this time?

Answer: In our study we only have estimates of DMS incidence in adult

broiler chicken stocks, e.g. 0 to 43% range for nine male parent stocks.

However, Richardson et al. (1980) reported a low incidence of DMS in

seven-week-old broiler chickens which had been handled a few days before

slaughter. I suggest that DMS is not commercially important now but could

be very important if age of onset of the disease is lowered to that ofbroiler chickens.

Question from Richard Frankham: Do you have an estimate of the heritabilityof liability to DMS?

Answer: Although I expected this question, I have not had time to calculate

the heritability of incidence to DMS, but expect to have an estimatesoon.

Question from Leonore Lasher: CK levels prior to exercise are much lower indiseased birds than non-DMS birds. Is this a significant difference? Is

it indicative of the presence of DMS? Could this measurement (CK prior

to exercise) be used in your selection program?

Answer: I did not test for the significance of this difference. Because of

the large variability and standard errors associated with the plasma CK

values prior to exercise, I doubt that these CK values would be indicative

of susceptibility to DMS or could be used in a selection program.

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