CHAPTER
8
Muscle
CHAPTER CONTENTS
Congenital/Developmental disorders 293
Non-infectious/traumatic disorders 297
Neoplastic disorders 303
Congenital/developmental disorders
Hyperkalemic periodic paralysis (HYPP) (Fig. 8.1)
This is a disease of Quarterhorses and their crosses. To date it has only
been traced to descendants of the stallion ‘Impressive’. It is transmit-
ted as an autosomal dominant trait. Most cases are seen in 2–3-year-
old well-muscled males but cases have been seen in foals as young as
4 months.
Heterozygotes and homozygotes show clinical signs, with signs
often being more severe and detected earlier in the latter. The most
common sign is muscle fasciculations. This can be followed by muscle
spasms, weakness and recumbency. Death can occur due to cardiac
or respiratory failure. Increased respiratory rates are common during
attacks. The pharyngeal and laryngeal muscles can also be affected
resulting in stridor or dyspnea.
Attacks may be precipitated by stressors such as transport, showing,
change in weather and general anesthesia. Hyperkalemia is common
during an attack although episodes without hyperkalemia have been
reported.
Diagnosis and treatment
• Definitive diagnosis is by genetic testing. This can be performed on
whole blood or hair root. The American Quarter Horse Association
(AQHA) will accept HYPP test results only if performed through a
licensed laboratory. Testing kits for non-registration purposes are
available from the AQHA.
• Diagnosed subjectively by clinical signs and signalment.
• Post-mortem samples that can be collected if a horse has died
during a suspected attack are: hair samples for DNA testing and
aqueous humor for potassium concentration.
• Mild cases can be treated with light exercise, by feeding a readily
absorbable source of carbohydrate (oats), and/or with acetazol-
amide (3 mg/kg orally).
• For severe cases, the following treatment is recommended: intra­
venous administration of 5% dextrose with sodium bicarbonate
(1–2 mEq/kg) and intravenous administration of 23% calcium glu-
conate (0.2–0.4 ml/kg ) diluted in 5% dextrose (4.4–6.6 ml/kg).
Control
• Management is an important feature of control and should include
regular exercise and ideally frequent paddock turnout. Wholegrain
feeds should be fed instead of sweet feed. Avoid feeds with high
potassium content such as alfalfa and replace with timothy or
Bermuda grass hay. Give several small feeds daily at regular
intervals.
• Avoid stressors such as rapid changes in diet, exposure to cold or
overexertion.
• Acetazolamide (2–4 mg/kg q 8–12 h) has been recommended to
decrease the frequency and severity of episodes. The daily dose can
be decreased over time until the lowest effective dose is reached.
Prognosis
The prognosis for normal activity is considered good. Counseling
about breeding such horses should be offered.
Myotonia congenita (Fig. 8.2)
Myotonia congenita is a rare condition of Quarterhorse (QH) and QH
cross foals that results in periods of involuntary muscle contractions
following stimulation or start of exercise. Affected animals usually
show clinical signs within the first year and often have well-developed
musculature and a pelvic limb stiffness/lameness. The well-muscled
appearance is similar to that seen in HYPP-affected animals.
Only the skeletal muscle is involved in myontonia congenita which
means that progression of clinical signs is not seen beyond 12 months
of age. A separate condition known as myotonic dystrophy has also
been reported in a QH foal. This condition progresses to severe muscle
atrophy and involvement of other organs.
Diagnosis
• Frequently a tentative diagnosis can be made on the basis of breed,
age and clinical signs.
• Definitive diagnosis requires EMG examination. The pathogno-
monic finding is described as crescendo-decresendo, high-frequency
repetitive bursts with a characteristic ‘dive-bomber’ sound.
• Muscle biopsies are not useful for diagnosis as they may be normal.
Treatment
• Most treatment modalities have poor efficacy. Phenytoin has been
used in a number of affected horses with reported success.
• Other drugs that may be beneficial are quinine and procainamide.
These are used to treat a similar condition in man and dogs.
Prognosis
• Depends on the severity of signs but is considered poor in most
cases.
• Some cases are mild and show a decrease in signs with age. Other
more severely affected animals may develop extensive fibrosis with
resultant restriction of movement.
• Some cases have also had concurrent HYPP.
Glycogen branching enzyme deficiency
This is an autosomal-recessive glycogen storage disorder that affects
neonatal Quarterhorses or Paint horses and has been identified in
294 Knottenbelt and Pascoe’s Color Atlas of Diseases and Disorders of the Horse

B C

Figure 8.1 (A–C) Typical heavily muscled body type associated with hyperkalemic periodic paralysis.
Differential diagnosis:
• Weakness, muscle fasciculations and collapse
• Generalized muscle weakness of neurological origin (e.g. equine degenerative myeloencephalopathy) or neuromuscular origin (e.g. botulism)
• Encephalitis (e.g. West Nile virus infection) (can cause muscle fasiculations)
• Electrolyte disorders (e.g. hypocalcemia)
• Exertional rhabdomyolysis
• Narcolepsy/cataplexy
• Syncope
• Seizures
• Nutritional myopathy
• Dyspnea
• Obstruction of the respiratory tract (e.g. foreign body)
• Pharyngeal/laryngeal paralysis (e.g. secondary to nerve damage in strangles cases).

aborted fetuses. As a result of the specific mutation certain
tissues such as the brain, liver, cardiac and skeletal muscle cannot
store and mobilize glycogen to maintain normal glucose hemo­
stasis. Approximately 8% of both Quarterhorses and Paint horses are
carriers of GBED. In one study 2–4% of aborted fetuses were homo-
zygous for GBED. The condition is likely underdiagnosed due to the
lack of readily available testing and the similarity in clinical signs
between this and many other neonatal conditions.
The most frequently encountered clinical signs are weakness, hypo-
thermia, hypoglycemia, flexural limb deformities and ventilatory
failure. None of these signs is pathognomonic and all are easily con-
fused with other conditions.
Diagnosis and treatment
• The most accurate form of diagnosis is through genetic testing but
there is currently limited availability.
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Figure 8.2 Myotonia congenita. Typical double muscled appearance. Many of the Figure 8.3 Polysaccharide storage myopathy. Note the firm muscles of the
affected horses are quarter horses which may also be affected with HYPP. hindquarters in this young Quarterhorse with type 1 PSSM.
Reproduced from McAuliffe SB, Slovis, NM (eds). Color Atlas of Diseases and
Disorders of the Foal (2008), with permission from Elsevier.
Differential diagnosis:
• HYPP
• Myotonic dystrophy
• PSSM type 1.

• Other findings are not consistent but include:

• Basophilic globules and eosinophilic crystalline material in
hematoxylin and eosin stains
• Periodic acid-Schiff (PAS) staining of cardiac and muscle sections
may contain PAS-positive globular inclusions.
• There is no effective treatment and therefore early identification and
euthanasia are is essential to avoid unnecessary costs in neonatal
care untis.
Polysaccharide storage myopathy (PSSM)
(Figs. 8.3 & 8.4)
This disorder is characterized by higher glycogen concentrations and
abnormal granular amylase-resistant inclusions in skeletal muscle.
There are two types of PSSM: type 1 PSSM refers to horses with a
specific glycogen synthase 1 gene (GYS1) mutation. This is commonly
found in Quarterhorses, draft horse breeds and their crosses; type 2
PSSM is not related to a mutation in GYS1 and occurs in Quarter-
horses and a large number of Warmblood breeds.
The clinical signs seen are somewhat breed-dependent:
• Quarterhorses. The most common signs are firm, painful
muscles, stiffness, fasciculations, weakness, sweating and reluc- Figure 8.4 Polysaccharide storage myopathy. Generalized weakness and inability
tance to move. The hindquarters are most commonly affected but to stand.
other muscles can also be involved. Signs of pain can be severe
and long-lasting. Signs can be seen with minimal work especially
in horses that have been rested for several days or are on a high- • Draft horses. Many affected horses do not have clinical signs.
grain diet. There is no specific association to gender, body type or Rhabdomyolysis and myoglobinuria can be seen in horses that
temperament. Average age of onset of clinical signs is 5 years but are fed high-grain diets, exercised irregularly or have little
signs have been seen in horses as young as 1 year of age. Serum turnout. Signs can also be seen with general anesthesia. Again
CK and AST activities are often persistently high in affected there is no gender predilection and the mean age of onset of clini-
horses with median values reported at 2 809 and 1 792 U/L, cal signs is 8 years. The median CK and AST levels in affected
respectively. horses are reported to be 459 and 537 U/L, respectively.
296 Knottenbelt and Pascoe’s Color Atlas of Diseases and Disorders of the Horse
• Warmbloods. Warmbloods may have either type 1 or type 2
PSSM depending on the crosses from which they are derived.
The most common clinical signs noted are painful, firm back
and hindquarter muscles. Overt rhabdomyolysis is not that
commonly seen. The mean age of onset is 8–11 years of age
and the median CK and AST activities are 323 and 331 U/L,
respectively.
Diagnosis and treatment
• Type 1 PSSM can be diagnosed through genetic testing which is
available through the University of Minnesota. Muscle biopsies
can also be used with the characteristic findings of amylase-
resistant granular polysaccharide in amylase periodic acid-Schiff
(PAS) stains.
• There is no genetic test available for type 2 and muscle biopsies
demonstrate increased or abnormal PAS-positive material that is
usually amylase-sensitive.
• However, because the diagnosis of PSSM based on muscle biopsies
alone is quite subjective it is important that the horse is thoroughly
evaluated to rule out other conditions.
• Episodes of rhabdomyolysis need specific treatment.
Management
• Horses with PSSM should ideally have some form of turnout
available.
• Exercise regimens should only be implemented after there has been
adequate time allowed for dietary changes (2 weeks). The duration
and not just the intensity of exercise is important and exercise
should be gradually introduced and consistently performed. It is
also important to minimize the number of days without some form
of exercise.
• Dietary management is very important in affected horses and
should first consist of reaching the ideal body weight for the horse.
Once this has been done the dietary modifications should combine
reducing glucose load and providing fat as an alternative energy
source. There are now a wide variety of commercially produced
diets available for horses with PSSM. The basic dietary principle is
that less than 10% of digestible energy (DE) be provided in the form
of starch and at least 13% in the form of fat.
Recurrent exertional rhabdomyolysis (RER)
There are many causes of exertional rhabdomyolysis in horses. The
term recurrent exertional rhabdomyolysis is used to describe one
form that appears to have a heritable basis in Thoroughbred horses.
The specific cause has not however been identified although it is
believed that there is abnormal regulation of intracellular calcium in
skeletal muscle. Clinical signs are more common in fillies especially
those with a nervous temperament. These signs include hindlimb
pain and lameness, high respiratory rate, sweating, a reluctance to
move and colic signs such as repeated pawing. These signs may last
several hours without treatment. Clinical signs are more frequently
seen in horses fed high-grain diets and concurrent lameness. The
type of exercise is also important with episodes being more common
in racehorses restrained to a slow canter, while post-race episodes are
infrequent. In some cases episodes can be seen without any exercise
or after transportation and in these cases may be more related to
temperament and nervousness associated with anticipated work or
racing.
Diagnosis
• Evaluation of serum CK and AST levels is used by many to identify
poor performance in association with subclinical episodes of RER.
In doing such tests it is important to be consistent with regard to
sampling times. The ideal is 4–6 hours after exercise but in many
cases due to yard management this is not possible and then samples
should be routinely collected at a standardized time in relation to
the previous day’s work.
• If serum muscle enzymes are normal but RER is still believed to be
a cause of poor performance an exercise test can be performed with
samples taken before and 4–6 hours after exercise. Exercise for such
tests should consist of 15 minutes of collected trotting. A 3–4-fold
rise in serum ck activity is indicative of subclinical muscle damage.
• While there is currently no genetic testing available for RER horses
it is an area of active research and such a test may be available in
the near future.
Treatment
• The goals of therapy for specific episodes of exertional rhabdomy-
olysis are relieving pain and anxiety, replacing fluid and electrolyte
losses and maintaining renal function.
• Non-steroidal anti-inflammatories are frequently used to relieve
pain and in mild cases may be the only treatment necessary.
However, they should be cautious or combined with intravenous
fluid therapy in dehydrated horses.
• Severely affected horses, dehydrated horses or horses with myoglo-
binuria should receive intravenous fluids. Hyperkalemia can occur
in some horses and can be treated by the administration of isotonic
sodium chloride. Some horses will be hypocalcemic and will require
supplementation with calcium.
• Other drug therapies include dantrium sodium (4 mg/kg PO q
4–6 h) which decreases muscle contracture and may help prevent
further muscle necrosis. Methocarbamol (a muscle relaxant)
(5–22 mg/kg IV slowly) produces variable results perhaps as a
reflection of the dose used. Corticosteroids are advocated by some
especially if the horse is recumbent. DMSO has been used as an
anti-oxidant, anti-inflammatory and osmotic diuretic. Tranquiliz-
ers may help relieve anxiety and the perpetuation of an episode.
Management
• Efforts to minimize stress for individual horses should be made; this
may include regular turnout perhaps with a companion, a regular
routine with regard to feeding and exercise and tailoring other
management factors for specific needs, e.g. some horses find the use
of mechanical walkers stressful while others may get overexcited if
handwalked.
• Exercise should be consistent and daily, avoiding trigger factors
such as fighting to maintain a certain speed.
• Feed programs should also be individually tailored with the recom-
mendation that less than 20% of DE be supplied by starch and at
least 15% be supplied by fat. Increasing the frequency of feeding
may help reduce anxiety associated with feeding and may also
encourage increased caloric intake in fussy feeders.
• Exercising horses require daily dietary supplementation with
sodium and chloride. This is provided in most cases by commercial
feeds but can also be provided by loose salt. Other electrolytes may
also be required, especially if horses are exercising in hot, humid
climates. Historically there have been supplements given with a
sodium bicarbonate base based on the former belief that lactic aci-
dosis contributed to exertional rhabdomyolysis. Given current
knowledge that this is not actually the case there is no basis for the
administration of such supplements.
• Various other medications such as tranquilizers, dantrium sodium,
phenytoin, hormones and thyroid supplements have been given
to horses with RER. The need for such medications should be
evaluated on an individual basis but it is important to remember
that many of these may result in positives in post-competition
doping tests.
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Malignant hyperthermia • The prognosis for athletic function is guarded, but is reported to be
This is a rare autosomal-dominant mutation of the skeletal muscle better in foals which respond well to initial therapy.
ryanodine receptor gene (RYR1) that results in marked hyperthermia Exertional rhabdomyolysis (Figs. 8.6 & 8.7)
and metabolic acidosis during inhalational anesthesia. Although most horses that will experience episodes of exertional
Diagnosis and treatment rhabdomyolysis have an underlying myopathy overexertion can lead
to rhabdomyolysis in any horse. It is particularly seen as part of the
• To date the condition has only been reported in Quarterhorses
exhausted horse syndrome in 3-day event and endurance horses.
and could be suspected in any horse of that breed showing
classical signs of lactic acidosis and hyperthermia (rectal temp Many of these horses will have multiple organ failure in addition to
>40°C). rhabdomyolysis as a result of a combination of factors including exer-
tion past their fitness level, fluid and electrolyte losses, depletion of
• There is a genetic test available from the University of Minnesota.
energy stores and extremes of environmental conditions.
• Pre-treatment with oral dantrolene sodium (4 mg/kg) 30–60
minutes prior to anesthesia is ideal but requires recognizing at-risk Diagnosis and treatment
horses. • The signs of rhabdomyolysis may be overshadowed by other signs
• Once an episode is underway there is little effective therapy; in exhausted horses where there is frequently a marked tachycardia
despite efforts to cool horses and treat acidosis with intravenous and tachypnea. Synchronous diaphragmatic flutter may be seen in
sodium bicarbonate the two reported cases both died of cardiac some cases as well as marked depression, dehydration, anorexia,
arrest. elevated body temperature, poor sweating response, ileus and
muscle cramps.
Non-infectious/traumatic disorders
Gastrocnemius muscle rupture (Fig. 8.5)
Rupture of the gastrocnemius muscle can occur in young foals as a
result of overextension while chasing the dam or as a foaling injury.
It can also occur secondary to severe flexor tendon laxity or tarsal
contracture.
Rupture of this muscle results in a typical crouched stance and
inability to bear weight on the affected limb. The gastrocnemius may
be markedly swollen secondary to hemorrhage. It is not uncommon
to see anemia secondary to blood loss. Foals have died acutely second-
ary to a severe gastrocnemius rupture and hemorrhage.
Treatment and prognosis
• Treatment most commonly involves placing a Thomas-Schroeder
splint for 1 month while confining the foal to stall rest. Following
removal of the splint box rest is required for a further month.
• Care should be taken in constructing the splint to ensure it is a
correct fit for the foal in question.
• Careful padding and regular reassessments are required to ensure
Figure 8.6 Exertional rhabdomyolysis. This is the sporadic form where this mare
that pressure sores do not develop.
was temporarily separated from her foal and ran her paddock for 20 minutes
• Tube casts can also be used but must be changed frequently and before they could be reunited. Soon afterwards the mare showed stiffness,
cast sores are inevitable. myoglobinuria and extreme hardening of the gluteal muscles.

Figure 8.5 Gastrocnemius muscle rupture. Reproduced from McAuliffe SB, Figure 8.7 Hardening of the muscles (more obvious on the left side) (same
Slovis, NM (eds). Color Atlas of Diseases and Disorders of the Foal (2008), with horse as Fig. 8.6).
permission from Elsevier.
298 Knottenbelt and Pascoe’s Color Atlas of Diseases and Disorders of the Horse
• Non-exhausted horses that have experienced exercise beyond their
fitness level will show pain and firmness of the back and hind leg
muscles in particular. There can be marked sweating and signs of
anxiety or colic.
• Laboratory findings in the exhausted horse can include metabolic
alkalosis, paradoxical aciduria, hypokalemia, hyponatremia, hypo-
chloremia, increases in CK, AST, LDH, proteinuria, azotemia, lipi-
dosis and elevations of serum creatinine and hepatic enzymes.
• In non-exhausted horses treatment is the same as other cases of
rhabdomyolysis (see p. 298).
• In exhausted horses early and aggressive fluid therapy is required.
Careful attention should be paid to electrolyte imbalances and their
correction and it is important to offer feed. Cooling of hyperthermic
horses is also important and is often best achieved by the use of cold
water body spray fans.
Post-anesthetic myelopathy (Fig. 8.8)
Post-anesthetic myelopathy has been reported in several young, heavy
horses. Halothane anesthesia was used in all cases. Signs ranged from
difficulty standing, to tetraplegia with flaccid paralysis and anesthesia
of the pelvic limbs. Affected horses became recumbent or remained
in lateral recumbency until euthanasia 1–8 days later. The syndrome
is thought to involve a number of factors including systemic arterial
hypotension, local venous congestion caused by halothane anesthesia
and compression of the caudal vena cava by abdominal viscera.
Diagnosis is based on history and clinical signs. The prognosis is
hopeless in the cases that have been described but milder cases may
not be recognized.
Post-anesthetic myopathy
Myopathy due to prolonged recumbency is relatively common, and
represents a complication of general anesthesia, in heavy horses in
particular. Characteristically the condition affects the dependent
muscles. Thus, heavy animals maintained in dorsal recumbency
develop an ischemic myopathy in the lumbar muscles, while the
muscles of one fore- or hindlimb (or both) may be affected in those
held in lateral recumbency for extended periods. The clinical features
of such a myopathy are obviously related to the specific muscles
affected and the extent of the damage. Affected muscle masses may
be hard, hot and grossly swollen but may, equally, be normal in
Figure 8.8 Post-anesthetic myopathy. Note the swelling of the gluteal muscles on
the right side.
appearance while being extremely painful and non-functional. In the
forelimb, the triceps mass is the most commonly affected and although
it is seldom grossly swollen as a result, muscle function is severely
compromised. Affected horses present with a lameness and weakness
which is very similar in appearance to radial paralysis. In some cases
there may also be components of neurological dysfunction at the
same time due to local nerve compression.
Diagnosis and treatment
• Typically, the onset of the clinical effects of these myopathies is
immediately or shortly after recovery from anesthesia and this aids
diagnosis.
• Muscle enzyme levels are almost always very elevated.
• Supportive care results in most horses responding well to therapy
and making a full recovery within 1–2 days.
• In rarer cases, especially where there has been local nerve damage,
some muscle atrophy may develop.
Traumatic injuries to the muscles (Figs. 8.9–8.15)
These are many and varied. Disruption of muscle masses without
concurrent breaks in the skin presents two major clinical syndromes.
Where the muscles of the abdominal wall are ruptured, an acquired
hernia (rupture) may develop. While in many cases these appear to
cause little difficulty, complications may arise when abdominal viscera
become entrapped within the hernia and more particularly when
these become incarcerated therein.
Rupture of muscles, occurring as a result of excessive or violent
contraction, may cause obvious distortion of the muscle belly itself
when there is simultaneous rupture of the muscle sheath (epimy-
sium). More often such disruption causes little overt swelling, with the
hemorrhage and disruption remaining within the sheath. Under
these circumstances, healing is accompanied by scarring, fibrosis and
possibly by calcification. Individual muscles undergoing fibrous meta-
plasia following this type of injury may ultimately become severely
wasted.
Diagnosis
• Clinical signs are sufficient for a diagnosis in cases of hernias but
ultrasonographic examination of the hernia contents may be
Figure 8.9 Abdominal muscle tears are most commonly traumatic in origin or
can be related to increased abdominal weight associated with late pregnancy or
hydrops of the fetal fluids. This mare had unsuccessfully tried to jump a gate, on
which she became hung from the backlegs with a resultant extensive tear of the
abdominal musculature and related hernia of abdominal contents. This photo was
taken 3 weeks after the initial injury.
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Figure 8.12 Tearing of the abdominal musculature may be difficult to

differentiate from tears of the prepubic tendon in mares in advanced pregnancy;
also, in many cases, both may co-exist. Cranial movement of the mammary gland
(as seen in this image) may help with differentiation, but ultrasonography should be
Figure 8.10 This horse presented with swelling over the lateral aspect of the performed to determine the extent of involvement of the musculature.
stifle. Ultrasound revealed a tear and hematoma of the quadriceps. The horse was
not lame. He was limited to hand walking for 2 weeks and made an uneventful
recovery.

Figure 8.11 A tear of the rectus abdominus muscle in a mare in late pregnancy.
There is a large amount of associated edema that makes the affected area appear
much larger than it actually is. Ultrasonographic imaging localized the tear to an
area of 20 cm in diameter. This mare was treated with placement of a belly band,
exercise restriction and anti-inflammatories. She later foaled with minimal
assistance.

Figure 8.13 Muscle tear with large intramuscular hematoma formation.

required, especially if the horse suddenly becomes painful or the
hernia dramatically increases in size or there is associated edema.
• Muscle rupture without herniation or swelling can be diagnosed
• Muscle tears or ruptures of other muscle masses may require spe-
ultrasonographically. Depending on the stage at which the horse is
cific physical therapy to avoid excess restriction associated with
examined there may be obvious hemorrhage within the muscle
fibrosis especially in competitive horses.
body or there may be evidence of fibrosis.
• More dramatic wounds, involving the laceration of skin and under-
Treatment lying muscles, are common in the horse. While the damage may
• Treatment for individual cases varies. Hernias may be closed surgi- look dramatic, the consequences are often surprisingly limited, with
cally either with sutures or with a mesh, depending on the size and healing and wound contracture occurring rapidly in the absence
location of the hernia. of complicating factors such as sequestration of bone or foreign
300 Knottenbelt and Pascoe’s Color Atlas of Diseases and Disorders of the Horse
Figure 8.14 Ultrasound image of the horse in Fig. 8.13 demonstrating a large
intramuscular hematoma.
Figure 8.15 Trauma with tearing and subsequent swelling of the common digital
extensor muscle.
matter, infection and/or excessive movement. Generally, wounds
involving large amounts of muscle are better prospects for sponta-
neous healing than those occurring in areas where no, or limited,
underlying muscle is present, such as the distal limb and those
wounds complicated by other damage such as to tendons and joints.
Muscle necrosis (Figs. 8.16–8.19)
There are many possible causes of muscle necrosis. These include:
infectious, toxic, nutritional, ischemic or in a large number of cases
idiopathic. The necrosis itself may be focal or generalized. Focal
Figure 8.16 (A, B) Injection site abscess. (A) Swelling over the affected area.
(B) Aspiration of abscess contents.
necrosis is commonly seen in foals after intramuscular administration
of drugs or following snake or spider bites.
Venomous snakes and spiders occur world-wide and the effects of
their toxins are varied. Many have profound neurological and/or
circulatory effects but many also have strong cytotoxic properties.
Most such bites are also infected by pathogenic bacteria and lead to
localized myonecrosis. As the effects of envenomation are closely
related to the volume of toxin injected relative to the weight of the
animal, few snake bites are capable of killing a horse directly but the
secondary effects of clostridial myonecrosis and swelling may have a
fatal result.
Necrosis and bacterial infection of muscle masses usually occur as
a result of infected wounds, or from iatrogenic damage following the
injection of irritant or caustic drugs. The injection of antibiotics
seldom results in local infection, but quite frequently intramuscular
injections result in local myonecrosis and infection subsequently
develops. The injection of other drugs more commonly results in
infected sites, and the most serious of these infections are those due
to Clostridium spp. bacteria, in which gas production and extensive
myonecrosis produce a life-threatening situation. Local damage of
this type within a muscle may have very serious immediate toxic
consequences, and affect the function of the specific mass of muscle,
adjacent nerves and blood vessels and other structures.
Muscle has a great capacity to regenerate, especially in young
animals and frequently a complete recovery is made. Extensive or
severe lesions may result in fibrosis of the muscle and permanent

Figure 8.17 Ultrasound image of the horse in Fig. 8.16 showing a large
intramuscular abscess (arrows).
A likely cause in horses which have fibrotic myopathy in one hindlimb
B
Figure 8.18 (A) Clostridial myonecrosis of the neck and head of a foal following
a poorly administered intramuscular injection. (B) The same foal imaged a number
of weeks later showing good healing but extensive scarring of the area.
Muscle
301
Figure 8.19 Ultrasound image of clostridial infection of the tongue secondary to
a wire foreign body. Note the hyperechoic gas echoes scattered through a pocket
of fluid which was consistent with a local anaerobic abscess.
deformity. Localized swelling and pain will be evident. If associated
with a limb there may be profound lameness.
Diagnosis and treatment
• A diagnosis can often be reached on the basis of history and clinical
signs. Imaging of the area affected, radiography or ultrasonography
depending on the site, reveals soft tissue swelling and may demon-
strate the presence of gas/air within the soft tissue. Culture any
discharge from draining tracts.
• Treatment involves supportive care, anti-inflammatories and anti-
microbials. In cases where anaerobic infections are thought to be
involved such as clostridial myonecrosis, fenestration of the area is
recommended.
Fibrotic myopathy
Traumatic damage to the semitendinosus, abscesses or local inflam-
mation of the semitendinosus or tearing of the insertion of the semi-
tendinosus which may occur for example during sliding stops in
reining horses can result in fibrotic myopathy. Damage to the semime-
branosus or gracilis can also result in the condition but these are less
common. Another cited cause is degenerative neuropathy causing
denervation of the distal semitendinosus. This is regarded as the most
with a progression to involve the other limb.
It is most often a unilateral condition and is not associated with any
pain or stress for the horse. The abnormal gait that accompanies the
condition is characteristic and diagnostic. There is a shortened cranial
phase of the stride with an abrupt ‘catching’ of the forward swing, a
slight caudal swing and a marked ‘slapping’ of the hoof to the ground.
This gait abnormality may be much less apparent at the trot and
canter. Affected horses may have a palpable thickening of the semi-
membranosus or semitendinosus muscles or an obvious dimpling or
depression of the affected area. Some horses will have an area of
osseous metaplasia that will be readily palpable.
The condition has also be seen in young foals and the etiology in
this group is unknown, although theories include traumatic insult
before, during or soon after delivery. Cases in foals are less likely to be
associated with palpable fibrosis.
Treatment
• There is no effective medical therapy.
• Surgical treatments include semitendinosus myotomy (resection
of the affected semitendinosus muscle), semitendinosus myotenec-
tomy (resection of affected muscle and tendon of insertion), or
302 Knottenbelt and Pascoe’s Color Atlas of Diseases and Disorders of the Horse
Figure 8.20 Immune-mediated polymyositis. Note the extensive muscle wastage
over the gluteal area.
Differential diagnosis:
• Other myopathies
• Neurogenic wastage from local nerve trauma
• Cachexia
• Poor nutrition.
semitendinosusectomy at the tibial insertion. All will result in
immediate gait improvement although myotomy and myotenec-
tomy are associated with a higher percentage of complications. At
least partial recurrence of the condition occurs in 30% of horses.
If a progressive neuropathy is involved in the pathogenesis then a
recurrence of signs is likely.
Immune-mediated myopathies (Fig. 8.20)
Three distinct myopathies with an apparent immune-mediated etiol-
ogy are recognized in horses:
• Acute rhabdomyolysis caused by S. equi
• Infarctive purpura hemorrhagica
• Immune-mediated polymyositis.
Acute rhabdomyolysis caused by S. equi
The majority of reported cases have been in Quarterhorses <7 years
of age. Affected horses usually have other concurrent evidence of
S. equi infection such as lymphadenopathy or guttural pouch
empyema. Initial clinical signs include a stiff gait that rapidly pro-
gresses to firm swollen and painful gluteal and epaxial muscles.
Recumbency follows quickly and most horses are euthanized within
48 h of presentation.
The exact pathogenesis is not known but may be related to a toxic-
shock-like syndrome caused by S. equi superantigens or local bactere-
mia with production of exotoxins or proteases.
Diagnosis
• The condition should be suspected based on clinical signs alone and
treatment instituted early.
• There are marked elevations of CK and AST. Titers to the M protein
of S. equi are low in affected horses unless there has been recent
vaccination for strangles. Titers to myosin-binding protein are typi-
cally high. Post-mortem examination reveals large areas of pale
necrotic lumbar and hindlimb muscles.
Treatment and prognosis
• There has been a high mortality rate in cases to date despite anti-
biotic therapy. A combination of rifampicin (which inhibits protein
synthesis) and penicillin is thought to be the best treatment
although reports are lacking.
• Additional treatments include non-steroidal anti-inflammatories
and high doses of short-acting corticosteroids, both of which may
help to control the inflammatory response.
• Because of the severe pain noted in affected horses constant rate
infusion of lidocaine, detomidine or ketamine may help reduce
anxiety and provide additional pain relief.
Infarctive purpura hemorrhagica
Affected horses present with painful lameness, muscle stiffness and/
or colic signs. There is normally a history of known exposure to S. equi
within the previous 3 weeks or elevated serum M-protein titers.
Classic signs of purpura hemorrhagica (PH) are present such as limb
edema and petechiation. Laboratory changes include marked eleva-
tions in CK and AST. Gastrointestinal infarction may result in eleva-
tion of WCC, RBC and total protein in peritoneal fluid. Biopsies of
abnormal muscle reveal diffuse acute coagulative necrosis. Post-
mortem examination shows extensive infarction and leukocytic vas-
culitis of skeletal musculature, skin, gastrointestinal tract and lungs.
The pathogenesis is thought to involve the deposition of immune com-
plexes in vessel walls. These complexes are primarily composed of IgM,
IgA and streptococcal M protein.
Diagnosis, treatment and prognosis
• Clinical signs combined with laboratory findings are used for diag-
nosis initially while awaiting biopsy results. Early recognition and
aggressive therapy may lead to a better outcome.
• High-dose methylprednisolone is used to treat a similar condition
in humans and could be combined with immunosuppressive agents
such as cyclophosphamide or azathioprine.
• While the prognosis with classic PH is normally good, cases
of infarctive PH have a poor prognosis. There is a report of suc­
cessful treatment of a horse with penicillin, non-steroidal anti-
inflammatories and corticosteroids.
Immune-mediated polymyositis
This condition is being increasingly reported in horses. Most affected
horses to date have been Quarterhorses with horses <8 years of
age or >16 years of age over-represented. Approximately one-third
of cases have had a history of previous exposure to S. equi. Clinical
signs include rapid-onset muscle atrophy of the back and croup
muscles. This atrophy may involve up to 50% of the affected muscle
mass within 1 week. Stiffness, malaise and weakness are also common
non-specific findings. In contrast to other immune-mediated myopa-
thies there are only mild to moderate elevations in muscle enzymes.
The pathogenesis of the condition remains unclear.
Diagnosis, treatment and prognosis
• Clinical signs and biopsy specimens of affected muscles which
reveal lymphocytic vasculitis, lymphocytic myofiber infiltration,
fiber necrosis with macrophage infiltration and regeneration.
• Horses with concurrent streptococcal infection should be treated
with antibiotics.
• Administration of corticosteroids normally results in rapid improve-
ment of clinical signs and prevents further muscle atrophy. Treat-
ment is required for at least 10 days and recurrence of muscle

atrophy requiring reintroduction of corticosteroids may be neces-
sary in some cases.
• The prognosis with treatment is good.
Atypical myopathy/pasture-associated
myopathy
This has been most frequently reported from the UK but has been seen
in other European countries and is also present in the US. The etiology
is an area of active investigation that is currently thought to be related
to a toxin produced by Box elder and Acer species of trees. There is
usually a history of recent (within the previous 4 days) grazing for at
least 6 hours a day. Several co-grazers may be affected simultaneously.
Clinical signs are acute in onset and include depression, weakness,
stiffness, recumbency, trembling, sweating and myoglobinuria.
Diagnosis and treatment
• The condition should be expected in any horse with suitable clinical
signs, history and geographical location. There are marked increases
in CK activity along with hypocalcemia, hyperglycemia and hyper-
lipemia. Histology reveals multifocal Zenkers necrosis. Urine of
affected horses has increased levels of acylcarnitines.
• Treatment is largely supportive in affected horses with mortality
rates of up to 85%. Unaffected grazing companions should be
removed for the pasture and fed concentrates/hay.
• Horses that have recovered have either made rapid full recoveries or
have had prolonged recoveries with marked muscle wastage.
Masseter myopathy (Fig. 8.21)
Masseter myopathy in which the masseter muscles become grossly
swollen and intensely painful is a rare disorder, affecting adult horses
kept under poor management and nutritional conditions. Affected
horses have an abrupt onset of anorexia; the masseter muscles are
obviously swollen and are intensely painful. Manipulation of the
mandible is resented strongly, and the lower jaw may be held slightly
open or firmly closed. Simultaneous cardiac and diaphragmatic dys-
Figure 8.21 Masseter myopathy.
Muscle
303
function (including synchronous diaphragmatic flutter) are fre-
quently seen.
Diagnosis and treatment
• Diagnosis is usually obvious clinically.
• Treatment involves improving the plane of nutrition and client
counseling in addition to anti-inflammatories and supportive care
if there is difficulty eating. Recovered horses may seem relatively
normal for a limited time, but profound masseter atrophy is a
common sequel.
Muscle atrophy (Fig. 8.22)
Loss of muscle mass in the horse may be a consequence of starvation
when the loss is general, but specific groups of muscles may undergo
atrophy in response to trauma, myopathy, denervation and chronic
disuse. Disuse atrophy is generally slow to develop whereas neuro-
genic atrophy, following total neurectomy, is much more rapid and
would be expected to affect all the muscles supplied by a particular
nerve. Disuse atrophy of muscles usually relates to underlying pain or
disability syndromes, often associated with a musculo-skeletal disor-
der. The identification of the cause of obvious and severe, longstand-
ing muscle atrophy may be particularly difficult.
Neoplastic disorders (Fig. 8.23)
Neoplastic conditions involving the muscles of the horse are rare, but
possible conditions include spindle cell tumors and primary sarcoma.
Occasionally individual muscles become affected by slow-growing
defects of structure which may resemble neoplastic changes. The
gross proliferation of a normal tissue type in an abnormal site such
as this is called a hamartoma. Their significance is usually related to
space-occupying compression of adjacent structures. A relatively
common site for muscle hamartoma formation is the semimembrano-
sus and semitendinosus muscles, and massive enlargement of these
may have secondary effects on bowel and urogenital function.
Diagnosis and treatment
• May be suspected on the basis of clinical appearance but biopsies
are generally required for a definitive diagnosis.
• Depending on the site and size, removal can be considered but nor-
mally their location and proximity to local vital structures preclude
removal.
Figure 8.22 Disuse atrophy of muscle associated with a pelvic fracture.
304 Knottenbelt and Pascoe’s Color Atlas of Diseases and Disorders of the Horse

References and further reading

Aleman, M., Brosnan, R.J., Williams, D.C., et al., 2005. Malignant Hyperther-
mia in horses anesthesized with halothane. J Vet Intern Med 19,
363–366.
McAuliffe, S.B., Slovis, N.M., 2008. Colour Atlas of Diseases and Disorders of
the Foal. WB Saunders, Philadelphia, PA, USA.
Reed, S.M., Bayly, W.M., Sellon, D.C., 2009. Equine Internal Medicine, third ed.
WB Saunders, St. Louis, MO, USA.
Robinson, N.E., Sprayberry, K.A. (eds.), 2009. Current Therapy in Equine
Medicine, sixth ed. WB Saunders, St. Louis, MO, USA.
Valberg, S.J., 2006. Polysaccharide storage myopathy: indepthmuscle disor-
ders. In: Proceedings. 52nd American association of Equine Practitioners,
pp. 365–372.

Figure 8.23 (A, B) Neoplasia. Muscular hamartoma.