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Muscular dystrophy-like disease in a thoroughbred foal
J. Comp.
Path.
1989
Muscular
Vol.
100
Dystrophy-like
T. Shirakawa,
Disease Foal
M. Ide, H. Taniyama, H. Oishi, T. Matsui
in a Thoroughbred
K. Tobiwatari, and T. Ono
H. Senba,
Department of Veterinary Pathology, Obihiro lJniversi[v of Agriculture and Veteterinacy Medicine, Obihiro, Hokkaido, Japan; and Hidaka Agricultural Aid, Mitsuishi. Hokkazdo, Japan
Summary
A l-month-old male thoroughbred foal, which had difficulty in walking, was killed and examined by histological, histochemical and ultrastructural methods. The muscles of the trunk and upper hind limbs were chiefly affected, and changes in the affected muscles resembled those in muscular dystrophy in man. The type of muscular dystrophy present in this foal and the significance of this disease in thoroughbred horses are discussed. The dystrophy in this foal resembled the limb-girdle type or myotonic dystrophy of muscular dystrophy in man. Introduction The muscular dystrophies in man involve a group of progressive, hereditary, degenerative diseases of the skeletal muscles, and they are subdivided into several types based on the mode of inheritance and clinical features (Dubowitz and Brooke, 1973; Walton and Gardner-Medwin, 1981; Kakulas and Adams, 1985). In recent years a muscular dystrophy-like disease resembling the human form has been reported in the dog (Whitney, 1958), mouse (Harman, Tassoni, Curtis and Hollinshead, 1963), chicken uulian and Asmundson, 1963)) sheep (McGavin and Baynes, 1969; McGavin, 1974; Dent, Richards and Nairn, 1977)) hamster (Homburger, 1972 ) , mink (Hegreberg, Comacho and Gorham, 1974), turkey (Sutherland, 1974), cow (Goedegebuure, Hartman and Hoebe, 1983) and cat (Vos, van der Linde-Sipman and Goedegebuure, 1986). They are indeed possible disease models for human muscular dystrophy. In” the present study, a male thoroughbred foal had muscular dystrophy, judging from the histopathological findings. Materials
and
Methods
A male thoroughbred foal was still incapable of walking at 2 days after birth and was suspected to be suffering from white muscle disease. The clinical signs progressed in spite of vitamin E and selenium treatments. The gluteal muscle became hard on Reprints ture and
request Veterinary
002 l-9975/89/030287
to ‘I‘akane Medicine,
Matsui, Department of Veterinary Inada-cho, Obihiro-shi, Hokkaido.
+ 08 $03.00/O
Pathology, Obihiro 080, Japan. 0
1989
University
Academic
of Agricul-
Press
Limited
288
T. Shirakawa
et al.
palpation and the posture at 1 month resembled that of a wooden horse. The foal was presented to our department since the prognosis was poor at this time, and was killed by exsanguination. At necropsy, tissue samples were collected from almost all organs and tissues, including brain and spinal cord, and fixed in 15 per cent formalin. All tissue samples were processed by conventional methods, embedded in paraffin wax, sectioned 4 pm thick and stained with haematoxylin and eosin (HE). Samples were collected from the central part of 23 muscles (Table 1). From each muscle sample, transverse and longitudinal sections were stained with HE, phosphotungstic-acid haematoxylin (PTAH) , periodic acid-Schiff (PAS), azan stain and Gomori’s reticulin methods. For electron microscopy, a portion of each muscle was fixed in 4 per cent paraformaldehyde in 0.5 M phosphate buffer, then fixed in 1.5 per cent osmium tetroxide and embedded in epoxy resin. Ultrathin sections were stained with uranyl nitrate followed by lead citrate. For histochemical examinations, fresh muscle samples of approximately 0.5 cm” were collected from the central part ot eight muscles (Table l), immersed in liquid nitrogen for about 15 s and stored at - 80°C until sectioned. Four 10 pm thick serial sections from each block were cut in a transverse plane with a cryostat and stained with HE, PAS, Gomori’s trichrome methods, myosin adenosine triphosphatase (ATP-ase) at pH 9.4 and 4.3 and reduced nicotinamide adenine dinucleotide-tetrazolium reductase (NADH-TR). Four muscles of a l-month-old male thoroughbred foal, which was killed because of another disease, were sampled as normal control muscle and processed as above (Table 1). In ATP-asr stained sections, a total of 200 fibres were measured in the lesser diameter, histograms were made of each fibre type (types I and 11) and the percentages of type I and II fibres were calculated.
Results At necropsy, the M. gluteus medius and M. sartorius were slightly pale and stiff on palpation, and the M. longissimus thoracis and M. triceps brachii were also slightly pale. The other organs and tissues were normal. Histologicaljndings There was no change in 14 muscles (Table 1). The fibres in these muscles were generally of equal size and arranged normally. The most prominent change was in the longissimus thoracis, gluteus medius and sartorius. In these muscles, the f&i-es varied markedly in size and were rounded or oval in shape (Fig. 1). There were many internal nuclei which were swollen and rounded and had a prominent nucleolus. Fibre-splitting and sarcoplasmic masses were often observed. The sarcoplasmic masses were slightly basophilic in HE stained sections, and negative for PAS. In azan and PTAH stained sections, the masses were clearly observed and often contained some myofibrils that were disconnected from the fibres. Ring fibres were often observed associated with the sarcoplasmic masses (Fig. 2). Perimysial connective tissues were slightly increased when stained by azan’, PTAH and Gomori’s reticulin methods. Necrotic fibres with phagocytosis and other degenerative changes were rarely observed and regenerating fibres were rare. These changes existed symmetrically in the muscles. In the other muscles, the fibre changes which were observed in the longissimus thoracis were also evident, but the lesions differed in a proportion of the same sections. No changes were observed in the central or peripheral nervous system, or other organs. Table 1 summarizes the changes in each muscle examined.
~~
carpi radialis rarpi ulnaris ,M. flexor carpi radialis M. flexor carpi ulnaris M. iliopsosa
M. M. M, M. M.
adductvres tibialis cranialis cstrnsor digitorum longus flexor digitorum sup&i&k gastro~nrmius
M. sartorius
M. biceps femoris ,&I. semitendinosus
.M. gluteus mrdius
M. extensor
M. extensor
of lesions
thoracis
brachii
M. biceps hrarhii
M. triceps
Diaphragma M. hulbi M. massrter M. longissiums M. deltoidrus
__
Presence
in various
-
+++
++
++ ++
A
+++
++
-
+++ -
hions
muscles,
variation
1 II I II
p/w
Fibre
in
fibre
size
1 number diameter
of type
f
9.45
4.54) 9.04)
I and
45.47 f 10.60 24.53 f 9.25 30.29f 12.50 121.46f 28.24f 7.43 ~38~00f 37.45f 13.03 (27.07f 30.15f 8.01 ‘31.48f
4.75, 11.21, 5.07) 7.39,
31.79* 10.70 38.00f Il.03 / 19.89f 4.541 30.44f 11.28 (30.29 f IO.041 23.61 f 3.28 29.04 f 5.77
27.39
Zl%Of 4.30 35.11 f 7.62 33.96f 9.86 (23.5Ozt 31.14f 12.29 (35.11 f
Mean jibre /mfSD
Table and
e
II fibres
233 377 413 263 348 266
(2211 1295, (1871 (235
345 338 290 (229; 371 (331 139 199
199 242 290 j 193) 391 (2571
Variabili!y coegicient
from
the
affected
and
control
5.7 94.3 34.5 (13.1, 6.5.i 86.9 68.3 : 29.2 1 11.7 ‘70.8’
28.8 71.2 73.1 9.51 26.9 ,9O.j 21.2 78.8
33.0 67.0 55.9 t, 16.61 44.1 (83.41
foal
T. Shirakawa
Fig.
I.
Fig.
2.
Fig.
3.
Fig. 5.
et al.
:d gluteus medius muscle. showing variation of tibre Transverse section of the most severly affec >osition, fibre splitting, sarcoplasmic mass. hyalinc size, prominent swollen nuclei in internal degeneration. HE x 400. ringed libre associated with sarcoplasmic Transverse section of semimembranosus mu rle, typical mass. Azan stain x 1000. of libre size, fibrc splitting (arrow), Fresh frozen section of gluteus medius muscl lc :, great variation normal mosaic pattern. ATP-ase at pH 9.4 :K 63. of type I fibres. ATP-ax at pH 9.4 Fresh frozen section of semitendionosus mw .I .e, predominance x 63.
Muscular
Dystrophy
in a Foal
291
Histochemicaljindings The muscle fibres were distinguishable as type I and type II by the ATP-ase reactions. Mean diameter, variability coefficient and percentage of type I and type II fibres are shown in Table 1. In the muscles of the control foal, type I and II fibres showed a mosaic pattern. Except for the deltoideus and rectus femoris, the other muscles in the affected foal showed individual muscle fibres which varied in size (Fig. 3). Except for the ilio-psoas, the mean diameter for type I fibres was larger than for type II fibres. The variation of fibre diameter in the control and affected muscles for types I and II, as well as the total fibres, is shown histographically (Fig. 4), and the histogram of fibre sizes shows a single peak for type I, type II, and overall fibres. The proportion of type I and II fibres differed from the control muscle, and type I fibre predominance was evident in the muscle compared with control muscles (Fig. 5). Fibre-splitting
Affected 200
m.
0 . . . . . . . . . . 0 Type1
-
.----.
Type
.-.
Total
Type
100
I
/
-
II
I: Mean S.D.
37.45 13.03
Meon S.D.
30.44 8.01
Typel3:
0.....0Type1 .----.
Type
A-.
Total
Type
1: Mean S.D.
27.0 5.07
TypelI:Mean
31.46 7.39
S.D.
1
I
I 20
I
I
I 40 Oiomcter
Fig. 4.
Histogram of fibre sizes in sartorius range distribution in affected foal.
muscle,
L 60
II
I
I 60
(pm)
single peak for typr
I, II and total fibres with
wide
292
T. Shirakawa
et
al.
was noted among type I and type II fibres, but was more prominent in type II fibres. Split fibres were stained identicaliy for histochemical type (Fig. 6). The areas of sarcoplasmic mass were basophilic in HE-stained sections and were
shownto have high NADH-TR
reactivity. Electron microscopically, the sarcoplasmic mass consisted of ribosomes, mitochondria and myofibrillar debris (Fig. 7 j. Ring fibres consisted of lihres with displaced myofibriis, or a group ofmyofibrils, at the fibre peripher!. The sarcoplasmic mass and the ring fibres frequently coexisted. Degenerative changes in the fibres of affected muscles were observed. but there were no other characteristic changes.
Discussion
Nutritional myopathy has been reported in foals in many countries, and this myopathy was histologically characterized by extensive floccular, granular and hyaline degeneration, followed by phagocytosis of necrotic fibres and abundant regeneration (Hadlow, 1973; Hulland, 1985; McEwen and Hulland, 1986). There were no histological resemblances to nutritional myopathy in the case of myopathy of the foal reported here, and no evidence of neurogenic disorder by histochemical (Dubowitz and Brooke, 1973) and histological findings. The histological changes of the present case were analogous to
Muscular
Dystrophy
in a Foal
293
muscular dystrophy in man. The dystrophies of man are subdivided into several types based on the mode of inheritance and clinical symptoms, but the essential changes in the muscles are histologically similar in all types ! Dubowitz and Brooke, 1973; Walton, 1973; Hughes, 1974; Kakulas and Adams, 198.5 i. It is suggested that the present case may have been affected by the limhgirdle type of muscular dystrophy -judging by the distribution of affected muscles, and also by myotonic dystrophy shown by numerous sarcoplasmic masses accompanied by myofibrillar disorganization (Dubowitz and Brooke, 1973; Kakulas and Adams, 1985). At the present time, the genetical background is not clear in the foal reported here, so the type of dystrophy must be determined by a survey of inherited factors. All thoroughbred horses are descended from only three male horses (Byerley Turk, Darley Arabian and Godolphin Barb) since about 1700 (Simpson, 195 1) . Therefore, genetically determined diseases are thought to exist. However, due to selection for racing ability, the congenital factors are unpublished and kept secret in
References Dent,
A. C., Richards, R. B. and Nairn, M. E. L,1977). Congenital progressive ovine muscular dystrophy in western Australia. Australian .Veterinar_y Journal, 55, 297. Dubowitz, V. and Brooke, M. H. (1973). In Muscle Biopsy: A Modern Approach. V. Dubowitz and M. H. Brooke, Eds, WB Saunders, London, Philadelphia, Toronto. Goedegebuure, S. A., Hartman, W. and Hoebe, H. P. (1983). Dystrophy of the Diaphragmatic Muscles in Adult Meuse-Rhine-Yssel Cattle: Elertoromyographical and Histological Findings. Veterinar_v Pathology, 120, 32-48. Hadlow, W. J. (1973). Myopathies of Animals. In The Striated Muscle. Carl M. Person and F. K. Mostofi, Eds. The Williams & Wilkins Company, Baltimore, pp. 364409. Harman, P. J., Tassoni, J. P., Curtis, R. L. and Hollinshead, ,M. B. (1963). Muscular dystrophy in the mouse. In Muscular Dystrophy in Man and Animals. G. H. Bourne and M. N. Golarz, Eds, Hafner Publishing Co., New York, pp. 407-457. Hegreberg, G. A., Comacho, Z. and Gorham, J. R. (1974). Histopathological description of muscular distrophy of mink. Archives of Pathology, 97, 225-229. Homburger, F. (1972). Disease models in Syrian hamsters. Progress in E.uperimental Tumor Research, 16, 69. Hughes, J. T. (1974). In Pathology of Muscle. J. T. Hughes, Ed., WB Saunders, Philadelphia, London, Toronto, pp. 73-93. Hulland, T. J. (1985). Muscles and tendons. In Pathology of Domestic Animals, Vol. 1, 3rd Edit. K. V. F. Jubb, P. C. Kennedy and N. Palmer, Eds, Academic Press, London, pp. 14&199. Julian, L. M. and Asmundson, V. S. (1963). Muscular dystrophy of the chicken. In Muscular Dystrophy in Man and Animals. G. H. Bourne and M. N. Golarz, Eds, Hafner Publishing Co., New York, pp. 457-498.
294
T. Shirakawa
et al.
Kakulas, B. A. and Adams, R. D. i 1985). III Disease of Muscle, Pathological Foundation oj Clinical Myology. B. A. Kakulas and R. D. Adams, Eds, Harper and Row, Philadelphia, pp. 368-459. McEwen, S. A. and Hulland, T. J. (1986). Histochemical and morphometric evaluation of skeletal muscle from horse with exrrtional rhahdomyolysis (Tying up). Lbterinary Pathology. 23, 400-4 10. MrGavin, M. I). (19741. Progressive ovine muscular dystrophy. Comparative Patholop Bulletin, 6, 3-10. McGavin, M. D. and Baynes, I. 1). (1969). A congenital progressive ovine muscular dystrophy. Veterinar?, Pathology, 6, 513 524. Simpson, G. G. ( 195 1) Somp European breeds in America. In Horses. G. G. Simpson. Ed., Oxford University Press, New York. Sutherland, I. R. (1974). Hereditary pectoral myopathy in the domestic turkey. Canadian Veterinarr Journal, 1.5, 7 7-8 1. \:os, J. H., van der Ilinde-Sipman and Goedegebuure, R. A. (1986). Dystrophy-like myopathy in the cat. Journal of‘Comparative Pathology, 96, 335-341. Walton, J. N. and Gardner-Medwin, D. (1981 j. Progressive muscular dystrophy and the myotonic disorders. In Disorders qf Voluntary Muscle, 4th Edit., .J. N. Walton, Ed., Churchill Livingstone, London, pp. 481-524. Walton, J. N. (1973). Progressive Muscular Dystrophy: Structural Alteration in Various Stages and in Carriers of Duchenne Dystrophy. In The Striated Muscle, Carl M. Pearson and F. K. Mostofi. Eds. Thr Williams & Wilkins Company, Baltimore, pp. 263 -291. Whitney, J. C. i 1958). Progressive muscular dystrophy in the dog. F’eterinarv Rurord, 70, 61 I. [ Rrceived.for publication.
November 30th, 1987 ]
Path.
1989
Muscular
Vol.
100
Dystrophy-like
T. Shirakawa,
Disease Foal
M. Ide, H. Taniyama, H. Oishi, T. Matsui
in a Thoroughbred
K. Tobiwatari, and T. Ono
H. Senba,
Department of Veterinary Pathology, Obihiro lJniversi[v of Agriculture and Veteterinacy Medicine, Obihiro, Hokkaido, Japan; and Hidaka Agricultural Aid, Mitsuishi. Hokkazdo, Japan
Summary
A l-month-old male thoroughbred foal, which had difficulty in walking, was killed and examined by histological, histochemical and ultrastructural methods. The muscles of the trunk and upper hind limbs were chiefly affected, and changes in the affected muscles resembled those in muscular dystrophy in man. The type of muscular dystrophy present in this foal and the significance of this disease in thoroughbred horses are discussed. The dystrophy in this foal resembled the limb-girdle type or myotonic dystrophy of muscular dystrophy in man. Introduction The muscular dystrophies in man involve a group of progressive, hereditary, degenerative diseases of the skeletal muscles, and they are subdivided into several types based on the mode of inheritance and clinical features (Dubowitz and Brooke, 1973; Walton and Gardner-Medwin, 1981; Kakulas and Adams, 1985). In recent years a muscular dystrophy-like disease resembling the human form has been reported in the dog (Whitney, 1958), mouse (Harman, Tassoni, Curtis and Hollinshead, 1963), chicken uulian and Asmundson, 1963)) sheep (McGavin and Baynes, 1969; McGavin, 1974; Dent, Richards and Nairn, 1977)) hamster (Homburger, 1972 ) , mink (Hegreberg, Comacho and Gorham, 1974), turkey (Sutherland, 1974), cow (Goedegebuure, Hartman and Hoebe, 1983) and cat (Vos, van der Linde-Sipman and Goedegebuure, 1986). They are indeed possible disease models for human muscular dystrophy. In” the present study, a male thoroughbred foal had muscular dystrophy, judging from the histopathological findings. Materials
and
Methods
A male thoroughbred foal was still incapable of walking at 2 days after birth and was suspected to be suffering from white muscle disease. The clinical signs progressed in spite of vitamin E and selenium treatments. The gluteal muscle became hard on Reprints ture and
request Veterinary
002 l-9975/89/030287
to ‘I‘akane Medicine,
Matsui, Department of Veterinary Inada-cho, Obihiro-shi, Hokkaido.
+ 08 $03.00/O
Pathology, Obihiro 080, Japan. 0
1989
University
Academic
of Agricul-
Press
Limited
288
T. Shirakawa
et al.
palpation and the posture at 1 month resembled that of a wooden horse. The foal was presented to our department since the prognosis was poor at this time, and was killed by exsanguination. At necropsy, tissue samples were collected from almost all organs and tissues, including brain and spinal cord, and fixed in 15 per cent formalin. All tissue samples were processed by conventional methods, embedded in paraffin wax, sectioned 4 pm thick and stained with haematoxylin and eosin (HE). Samples were collected from the central part of 23 muscles (Table 1). From each muscle sample, transverse and longitudinal sections were stained with HE, phosphotungstic-acid haematoxylin (PTAH) , periodic acid-Schiff (PAS), azan stain and Gomori’s reticulin methods. For electron microscopy, a portion of each muscle was fixed in 4 per cent paraformaldehyde in 0.5 M phosphate buffer, then fixed in 1.5 per cent osmium tetroxide and embedded in epoxy resin. Ultrathin sections were stained with uranyl nitrate followed by lead citrate. For histochemical examinations, fresh muscle samples of approximately 0.5 cm” were collected from the central part ot eight muscles (Table l), immersed in liquid nitrogen for about 15 s and stored at - 80°C until sectioned. Four 10 pm thick serial sections from each block were cut in a transverse plane with a cryostat and stained with HE, PAS, Gomori’s trichrome methods, myosin adenosine triphosphatase (ATP-ase) at pH 9.4 and 4.3 and reduced nicotinamide adenine dinucleotide-tetrazolium reductase (NADH-TR). Four muscles of a l-month-old male thoroughbred foal, which was killed because of another disease, were sampled as normal control muscle and processed as above (Table 1). In ATP-asr stained sections, a total of 200 fibres were measured in the lesser diameter, histograms were made of each fibre type (types I and 11) and the percentages of type I and II fibres were calculated.
Results At necropsy, the M. gluteus medius and M. sartorius were slightly pale and stiff on palpation, and the M. longissimus thoracis and M. triceps brachii were also slightly pale. The other organs and tissues were normal. Histologicaljndings There was no change in 14 muscles (Table 1). The fibres in these muscles were generally of equal size and arranged normally. The most prominent change was in the longissimus thoracis, gluteus medius and sartorius. In these muscles, the f&i-es varied markedly in size and were rounded or oval in shape (Fig. 1). There were many internal nuclei which were swollen and rounded and had a prominent nucleolus. Fibre-splitting and sarcoplasmic masses were often observed. The sarcoplasmic masses were slightly basophilic in HE stained sections, and negative for PAS. In azan and PTAH stained sections, the masses were clearly observed and often contained some myofibrils that were disconnected from the fibres. Ring fibres were often observed associated with the sarcoplasmic masses (Fig. 2). Perimysial connective tissues were slightly increased when stained by azan’, PTAH and Gomori’s reticulin methods. Necrotic fibres with phagocytosis and other degenerative changes were rarely observed and regenerating fibres were rare. These changes existed symmetrically in the muscles. In the other muscles, the fibre changes which were observed in the longissimus thoracis were also evident, but the lesions differed in a proportion of the same sections. No changes were observed in the central or peripheral nervous system, or other organs. Table 1 summarizes the changes in each muscle examined.
~~
carpi radialis rarpi ulnaris ,M. flexor carpi radialis M. flexor carpi ulnaris M. iliopsosa
M. M. M, M. M.
adductvres tibialis cranialis cstrnsor digitorum longus flexor digitorum sup&i&k gastro~nrmius
M. sartorius
M. biceps femoris ,&I. semitendinosus
.M. gluteus mrdius
M. extensor
M. extensor
of lesions
thoracis
brachii
M. biceps hrarhii
M. triceps
Diaphragma M. hulbi M. massrter M. longissiums M. deltoidrus
__
Presence
in various
-
+++
++
++ ++
A
+++
++
-
+++ -
hions
muscles,
variation
1 II I II
p/w
Fibre
in
fibre
size
1 number diameter
of type
f
9.45
4.54) 9.04)
I and
45.47 f 10.60 24.53 f 9.25 30.29f 12.50 121.46f 28.24f 7.43 ~38~00f 37.45f 13.03 (27.07f 30.15f 8.01 ‘31.48f
4.75, 11.21, 5.07) 7.39,
31.79* 10.70 38.00f Il.03 / 19.89f 4.541 30.44f 11.28 (30.29 f IO.041 23.61 f 3.28 29.04 f 5.77
27.39
Zl%Of 4.30 35.11 f 7.62 33.96f 9.86 (23.5Ozt 31.14f 12.29 (35.11 f
Mean jibre /mfSD
Table and
e
II fibres
233 377 413 263 348 266
(2211 1295, (1871 (235
345 338 290 (229; 371 (331 139 199
199 242 290 j 193) 391 (2571
Variabili!y coegicient
from
the
affected
and
control
5.7 94.3 34.5 (13.1, 6.5.i 86.9 68.3 : 29.2 1 11.7 ‘70.8’
28.8 71.2 73.1 9.51 26.9 ,9O.j 21.2 78.8
33.0 67.0 55.9 t, 16.61 44.1 (83.41
foal
T. Shirakawa
Fig.
I.
Fig.
2.
Fig.
3.
Fig. 5.
et al.
:d gluteus medius muscle. showing variation of tibre Transverse section of the most severly affec >osition, fibre splitting, sarcoplasmic mass. hyalinc size, prominent swollen nuclei in internal degeneration. HE x 400. ringed libre associated with sarcoplasmic Transverse section of semimembranosus mu rle, typical mass. Azan stain x 1000. of libre size, fibrc splitting (arrow), Fresh frozen section of gluteus medius muscl lc :, great variation normal mosaic pattern. ATP-ase at pH 9.4 :K 63. of type I fibres. ATP-ax at pH 9.4 Fresh frozen section of semitendionosus mw .I .e, predominance x 63.
Muscular
Dystrophy
in a Foal
291
Histochemicaljindings The muscle fibres were distinguishable as type I and type II by the ATP-ase reactions. Mean diameter, variability coefficient and percentage of type I and type II fibres are shown in Table 1. In the muscles of the control foal, type I and II fibres showed a mosaic pattern. Except for the deltoideus and rectus femoris, the other muscles in the affected foal showed individual muscle fibres which varied in size (Fig. 3). Except for the ilio-psoas, the mean diameter for type I fibres was larger than for type II fibres. The variation of fibre diameter in the control and affected muscles for types I and II, as well as the total fibres, is shown histographically (Fig. 4), and the histogram of fibre sizes shows a single peak for type I, type II, and overall fibres. The proportion of type I and II fibres differed from the control muscle, and type I fibre predominance was evident in the muscle compared with control muscles (Fig. 5). Fibre-splitting
Affected 200
m.
0 . . . . . . . . . . 0 Type1
-
.----.
Type
.-.
Total
Type
100
I
/
-
II
I: Mean S.D.
37.45 13.03
Meon S.D.
30.44 8.01
Typel3:
0.....0Type1 .----.
Type
A-.
Total
Type
1: Mean S.D.
27.0 5.07
TypelI:Mean
31.46 7.39
S.D.
1
I
I 20
I
I
I 40 Oiomcter
Fig. 4.
Histogram of fibre sizes in sartorius range distribution in affected foal.
muscle,
L 60
II
I
I 60
(pm)
single peak for typr
I, II and total fibres with
wide
292
T. Shirakawa
et
al.
was noted among type I and type II fibres, but was more prominent in type II fibres. Split fibres were stained identicaliy for histochemical type (Fig. 6). The areas of sarcoplasmic mass were basophilic in HE-stained sections and were
shownto have high NADH-TR
reactivity. Electron microscopically, the sarcoplasmic mass consisted of ribosomes, mitochondria and myofibrillar debris (Fig. 7 j. Ring fibres consisted of lihres with displaced myofibriis, or a group ofmyofibrils, at the fibre peripher!. The sarcoplasmic mass and the ring fibres frequently coexisted. Degenerative changes in the fibres of affected muscles were observed. but there were no other characteristic changes.
Discussion
Nutritional myopathy has been reported in foals in many countries, and this myopathy was histologically characterized by extensive floccular, granular and hyaline degeneration, followed by phagocytosis of necrotic fibres and abundant regeneration (Hadlow, 1973; Hulland, 1985; McEwen and Hulland, 1986). There were no histological resemblances to nutritional myopathy in the case of myopathy of the foal reported here, and no evidence of neurogenic disorder by histochemical (Dubowitz and Brooke, 1973) and histological findings. The histological changes of the present case were analogous to
Muscular
Dystrophy
in a Foal
293
muscular dystrophy in man. The dystrophies of man are subdivided into several types based on the mode of inheritance and clinical symptoms, but the essential changes in the muscles are histologically similar in all types ! Dubowitz and Brooke, 1973; Walton, 1973; Hughes, 1974; Kakulas and Adams, 198.5 i. It is suggested that the present case may have been affected by the limhgirdle type of muscular dystrophy -judging by the distribution of affected muscles, and also by myotonic dystrophy shown by numerous sarcoplasmic masses accompanied by myofibrillar disorganization (Dubowitz and Brooke, 1973; Kakulas and Adams, 1985). At the present time, the genetical background is not clear in the foal reported here, so the type of dystrophy must be determined by a survey of inherited factors. All thoroughbred horses are descended from only three male horses (Byerley Turk, Darley Arabian and Godolphin Barb) since about 1700 (Simpson, 195 1) . Therefore, genetically determined diseases are thought to exist. However, due to selection for racing ability, the congenital factors are unpublished and kept secret in
References Dent,
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