J Vet Intern Med 2004;18:679–691

Canine Inflammatory Myopathies: A Clinicopathologic Review of

200 Cases
Jason Evans, Donald Levesque, and G. Diane Shelton

A retrospective study was performed on 200 randomly selected cases of inflammatory myopathy in dogs from diagnostic muscle
biopsies received at the Comparative Neuromuscular Laboratory, University of California, San Diego. The most common clinical
signs in dogs diagnosed with an inflammatory myopathy were generalized weakness, stilted gait, dysphagia, masticatory or gen-
eralized muscle atrophy, inability to open the jaw, megaesophagus, and dysphonia. Myalgia was rarely described. Age of onset
ranged from 0.25 to 14 years. Genders were equally represented. Breed distribution approximated the 2002 American Kennel Club
registration statistics (r 5 .85) with the notable exception of Boxers and Newfoundlands. From the results of muscle biopsies,
clinical signs, and presence or absence of antibodies against type 2M fibers, dogs were classified as a generalized inflammatory
myopathy (gIM)—including immune-mediated polymyositis; infectious and preneoplastic myositis; and, rarely, dermatomyositislike
or overlap syndromes or unclassified myositis—or a focal inflammatory myopathy (fIM)—including masticatory muscle and ex-
traocular myositis. Average creatine kinase (CK) and aspartate aminotransferase (AST) concentrations in gIMs were significantly
higher than those with fIMs (P , .05). Neoplasia developed in 12 of 200 dogs within 12 months of diagnosis of polymyositis,
with lymphoma diagnosed in 6 of 32 Boxers. Inflammatory myopathy was associated with antibody titers against infectious diseases
in 38 dogs. Neospora caninum and Hepatozoon americanum cysts were found in tissues of 2 dogs not serologically tested.
Antibodies against an unidentified sarcolemmal antigen were found in 9 of 19 Newfoundlands with polymyositis. The spectrum
of canine inflammatory myopathies can be broad, with infectious etiologies relatively common, and can include preneoplastic and
uncharacterized syndromes.
Key words: Dermatomyositis, Extraocular myositis, Masticatory muscle, Polymyositis.

I nflammatory myopathies are a heterogeneous group of

disorders characterized by nonsuppurative cellular in-
filtration of skeletal muscle.1 The term polymyositis has
been used in both human and veterinary medicine to de-
scribe generalized inflammatory myopathies regardless of
etiology. In human medicine, the term specifically is re-
served for myositis of presumed immune-mediated etiolo-
gy. For consistency, the term generalized inflammatory my-
opathy (gIM) is used in this report as a general description
for diffuse inflammatory myopathies, including infectious
and preneoplastic syndromes, and the term focal inflam-
matory myopathy (fIM) is used for the localized syn-
dromes. Dermatomyositislike, unclassified, and overlap
syndromes will be characterized separately. Both general-
ized and focal forms of inflammatory myopathies have been
reported in the dog.
Generalized inflammatory myopathies include polymyo-
sitis (PM),2 an immune-mediated disorder with diagnostic
criteria, including clinical signs of muscle weakness, stilted
gait, and muscle atrophy; abnormally high serum creatine
kinase (CK) concentrations; abnormal electromyography
(EMG); negative serologic tests for infectious disease; and
histologic confirmation of lymphocytic infiltrates in skeletal
muscle.3 gIMs also have been associated with infectious
agents, including protozoa,4–11 as well as rickettsia,12,13 spi-
rochetes,14 and other bacteria.15,16 Recent evidence has con-
From the Veterinary Neurological Center, Las Vegas, NV 89108
(Evans, Levesque); and the Department of Pathology, University of
California, San Diego, La Jolla, CA (Shelton). Portions of this study
presented at the 2003 ACVIM Forum in Charlotte, NC.
Reprint requests: Dr Jason Evans, Veterinary Neurological Center,
4445 N Rainbow Boulevard, Las Vegas, NV 89108; e-mail:
DrJasonDVM@aol.com.
Submitted February 9, 2004; Revised March 29, 2004; Accepted
April 22, 2004.
Copyright q 2004 by the American College of Veterinary Internal
Medicine
0891-6640/04/1805-0014/$3.00/0
firmed an association between malignancy and inflamma-
tory myopathies in humans.17 In dogs, a few reports also
have associated inflammatory myopathies with neoplasia,
including bronchogenic carcinoma, myeloid leukemia, ton-
sillar carcinoma, and other malignancies.18,19
Focal inflammatory myopathies include masticatory
muscle myositis (MMM)3,20–23 and extraocular myositis
(EOM),24 with cellular infiltrates restricted to these partic-
ular muscle groups. The most common clinical signs as-
sociated with MMM are inability to open the jaw, jaw pain,
and masticatory muscle atrophy. Cellular infiltrates in
MMM selectively affect the muscles innervated by the
mandibular branch of the trigeminal nerve, including the
masseter, temporalis, pterygoids, tensor tympani, and tensor
veli palatini muscles.25 Masticatory muscles contain a
unique muscle fiber type, type 2M, that differs both histo-
chemically25 and biochemically26 from fiber types present
in limb muscles. A recent study suggested that an immu-
nologically distinct microenvironment also might be present
in masticatory muscles compared with limb muscles.27 In
PM, CD81 cells were present in greater numbers than
CD41 cells, T cells used predominantly the ab T-cell re-
ceptor, and no B cells were found. In MMM, CD41 cells
were present in greater numbers than CD81 cells, T lym-
phocytes utilized both ab and gd receptors, and multifocal
clusters of B lymphocytes were present.27 Antibodies
against masticatory muscle type 2M fibers also have been
consistently associated with MMM.20
Extraocular myositis is a fIM with clinical signs restrict-
ed to the extraocular muscles with sparing of the mastica-
tory and limb muscles.24 The immune response might be
directed against unique antigens associated with this muscle
group. Bilateral exophthalmos from swelling of the extra-
ocular muscles is the only clinical sign in EOM. Exoph-
thalmos also can be found in MMM but, when present, is
a result of swelling of the pterygoid muscle and not the
extraocular muscles.23,24 Serum antibody titers for antibod-
680 Evans et al
ies against masticatory muscle type 2M fibers are negative
in EOM.
Dermatomyositis, first described in Collies, is an uncom-
mon immune-mediated generalized inflammatory disorder
affecting the skin, skeletal muscle, and vasculature.28–30
Dermatomyositis most commonly occurs in Collies and
Shetland Sheepdogs,31,32 but sporadic cases have been de-
scribed in other breeds.33 Although not yet documented in
dogs, dermatomyositis associated with malignancy fre-
quently has been reported in humans.1,17
The purpose of this study was to further classify canine
inflammatory myopathies and determine the relative fre-
quencies and breed predispositions of the various syn-
dromes, etiologies, and long-term outcomes on the basis of
the summary findings of signalment, clinical signs, histo-
pathologic descriptions, clinicopathologic findings, and se-
rologic tests. Data was compiled and analyzed from 200
dogs previously diagnosed with an inflammatory myopathy
on the basis of muscle biopsy evaluation.
Methods and Materials
Histopathology and Histochemistry
Biopsy specimens from dogs with clinical signs consistent with
muscle disease were collected by practicing veterinarians throughout
the United States through an open surgical biopsy procedure. The most
commonly submitted muscles for histopathologic evaluation included
the temporalis and masseter muscles for suspected MMM; the lateral
rectus muscle for suspected EOM; and the triceps brachii, vastus la-
teralis, cranial tibial, biceps femoris, and gastrocnemius muscles for
generalized disorders. Infrequently submitted muscles included the su-
praspinatus, a laryngeal muscle, deltoideus, biceps brachii, semimem-
branosis, infraspinatus, and extensor carpi radialis.
After shipment of cold tissue to the Comparative Neuromuscular
Laboratory at the University of California, San Diego, muscle speci-
mens were snap frozen in isopentane, precooled in liquid nitrogen, and
stored at 2808C until evaluation. All muscles submitted to the labo-
ratory were evaluated with a standard panel of histochemical stains
and reactions as described by Dubowitz.34 Routine histopathology was
performed on frozen muscle sections with the hematoxylin and eosin
and modified Gomori trichrome stains. Macrophages were identified
within cellular infiltrates with the use of the acid phosphatase stain,
and eosinophils were identified by the peroxidase reaction.
Case Selection
Two hundred randomly selected dogs from the tissue archives of
the Comparative Neuromuscular Laboratory, previously diagnosed
with an inflammatory myopathy on the basis of evaluation of muscle
biopsy specimens between 1995 and 2002, were retrospectively ana-
lyzed. Information including signalment, patient history, presenting
clinical signs, results of neurologic examinations, clinicopathologic
and serologic findings, electrodiagnostic evaluation, individual medical
treatment, and patient follow-up was obtained from the sample sub-
mission forms, and follow-up questionnaires were completed by the
submitting veterinarians.
Clinicopathologic Evaluation
Minimum databases, including CBC, biochemical analyses, and rou-
tine serologic tests, were performed at various commercial diagnostic
laboratories by standard procedures. Data regarding white blood cell
count, serum CK, aspartate aminotransferase (AST) and alanine ami-
notransferase (ALT) activities, total thyroxine concentrations, antinu-
clear antibody titer, and Coombs’ and rheumatoid factor tests were
obtained from the submission form or questionnaire. Antibody titers
against masticatory muscle type 2M fibersa and acetylcholine recep-
torsb were performed at the Comparative Neuromuscular Laboratory
by methods described previously.21,35
Results of serologic testing for Toxoplasma gondii, Neospora can-
inum, Borrelia burgdorferi, Ehrlichia cania, and Rickettsia rickettsii
specifically were requested on the questionnaire. Although reference
values for the respective tests for infectious organisms varied among
different commercial or institutional laboratories, antibody titers were
considered positive if the titer was higher than the lowest positive
result expected by previous exposure or vaccination as described in
published reports.36–39 Myositis was classified as associated with an
infectious agent if serum from an affected dog was positive for cir-
culating antibodies to the agent and clinical signs responded to appro-
priate antimicrobial medication or if an organism was identified on
muscle biopsy specimens or at postmortem examination.
Electrodiagnostic Testing
Electrophysiologic testing was performed by standard procedures40
at several sites. Results of EMG and motor nerve conduction velocity
(NCV) studies performed during the diagnostic workup of dogs with
a suspected inflammatory myopathy were obtained from the submis-
sion form and questionnaire.
Clinical Outcome
Recovery was defined as the time from diagnosis to when dogs had
shown clinical improvement but still were on medical therapy for clin-
ical signs of an inflammatory myopathy. Normal was defined as the
time to resolution of clinical signs and the discontinuation of medi-
cations for treatment of the inflammatory myopathy. The time from
onset of clinical signs to diagnosis (ie, muscle biopsy), the time to
recovery or to normal, or the time to death was determined from the
submission form and follow-up questionnaire.
Statistical Analysis
All statistical comparisons between groups were made by Student’s
t-test. The level of significance chosen was P , .05. Correlation anal-
ysis was applied to a scatterplot to measure the correlation coefficient
(r) of the relationship between the percent population distribution of
breeds in the study compared with the percent population distribution
of breeds of the general population as reported by 2002 American
Kennel Club (AKC) registrations.
Results
Classification of Canine Inflammatory Myopathies
Classification was based on a combination of histopath-
ologic confirmation of the inflammatory myopathy, gener-
alized or focal clinical signs, results of serologic testing for
infectious diseases, and results of the 2M antibody test. gIM
(140/200, 70%; Fig 1A) and MMM (45/200, 22.5%; Fig
1B) were most frequently diagnosed. Small numbers of
dogs had an overlap syndrome in which cellular infiltration
was present in both masticatory muscle and limb muscle
biopsies, and antibodies were detected against type 2M fi-
bers (3/200, 1.5%). gIMs were further classified to include
(1) immune-mediated PM in 88 of 140 (63%) dogs, (2) an
infectious etiology in 40 of 140 (28.5%) dogs, and (3) a
preneoplastic syndrome in 12 of 140 (8.5%) dogs. For the
dogs with preneoplastic syndrome, tumor cells were not
identified in the original biopsies but were detected in re-
peat muscle specimens up to 12 months after the original
diagnosis. Other infrequent diagnoses included dermato-
 Canine Inflammatory Myopathies 681

Fig 1. Muscle biopsies are shown from dogs with various inflammatory myopathies, including immune-mediated polymyositis (A), masticatory
muscle myositis (B), and uncharacterized myositides associated with a necrotizing vasculitis (C) (star indicates necrotic vessel wall, the lumen
is occluded), and macrophagic myositis with noncaseating granulomas (D). Hematoxylin-eosin. Bar 5 109 mm for all parts.

myositislike syndrome (3/200, 1.5%), EOM (2/200, 1%), or
an unclassified myositis (7/200, 3.5%).
Dogs with clinical signs and histopathologic findings in
muscle biopsies not typical of the traditional classifications
of an inflammatory myopathy were diagnosed with an un-
classified myositis. All dogs in this category had negative
serology results for infectious diseases as well as negative
2M antibody titers. Unclassified myopathies included those
associated with necrotizing vasculitis (Fig 1C) or granulo-
matous myositis (Fig 1D).
Signalment
A summary of age, gender, and time from onset of clin-
ical signs to diagnosis and recovery for 200 dogs with an
inflammatory myopathy is shown in Table 1; the common
gIM classifications are shown in Table 2. A gender predi-
lection for an inflammatory myopathy was not evident. The
overall mean age for all dogs was 4.88 6 2.8 years. Sig-
nificant differences (P , .05) were found for dogs with
overlap syndrome (1.33 6 0.33 years), dermatomyositislike
syndrome (7.6 6 1.7 years), and infection with N caninum
(3.22 6 2.3 years). The mean time to diagnosis (ie, biopsy)
after the onset of clinical signs for dogs with gIM (18.17
6 24.9 weeks) and overlap syndrome (14 6 15.8 weeks)
was significantly different from dogs with MMM (6.8 6
9.1 weeks), dermatomyositislike syndrome (3 6 1.4
weeks), EOM (1 6 0.0 week), and an unclassified myop-
athy (4.57 6 2.9 weeks) compared with other groups (P ,
.05). This finding might reflect more distinguishable clinical
signs in the latter groups, resulting in earlier diagnostic test-
ing.
The 50 breeds represented in this study and the mean age
for each breed are listed in Table 3. The distribution of
listed breeds correlated with the distribution of the general
population as reported by 2002 AKC registrations (r 5 .85)
with the exception of Boxers (n 5 32) and Newfoundlands
(n 5 19), which were overrepresented (Fig 2). In addition,
the Airedale (0.25 6 0.0 years), Akita (2 6 0.0 years),
Briard (2 6 0.0 years), Brittany Spaniel (2 6 0.0 years),
Chihuahua (4 6 0.0 years), English Bulldog (3.5 6 3.1
years), Fox Terrier (3 6 1.0 years), Malamute (2 6 0.0
years), Mastiff (3.5 6 0.7 years), Newfoundland (2.1 6 1.1
682 Evans et al

Table 1. Age, sex, and clinical outcome for 200 dogs with an inflammatory myopathy.a
gIM MMM OS DM EOM UN Total
Number in study 140 45 3 3 2 7 200
Age (years) 5.09 6 2.6 4.47 6 3.3 1.33 6 0.3 7.6 6 1.7 4.5 6 4.9 3.9 6 2.4 4.88 6 2.8
Range 0.25–12 1–14 1–1.5 5–11 1–8 1.5–7.5 0.25–14
Gender
MN 48 12 2 3 66
FS 52 19 3 2 2 78
M 23 10 2 33
F 17 4 1 23
Onset (weeks) 18.17 6 24.9 6.8 6 9.1 14 6 15.8 3 6 1.4 1 6 0.0 4.57 6 2.9 14.3 6 21.7
Range 1–156 1–52 2–32 2–4 1–12 1–156
n 103 37 3 2 2 7 154
Recovery (weeks) 29.7 6 27.9 16.4 6 17.9 12 6 0.0 8 6 0.0 22.7 6 33.1
Range 1–104 2–52 1–104
n 46 31 1 1 2 81
Normal (weeks) 9.5 6 9.1 6 6 5.2 12 6 0.0 6 6 0.0
Range 1–104 2–12 1–104
n 28 9 1 1 39
Died (weeks) 14.2 6 19.2 104 6 0.0
Range 1–56
n 9 1 10
Euthanized (weeks) 15.6 6 17.8 52 6 0.0 22.6 6 33.1
Range 1–104 1–130
n 24 1 2 27
Lost to follow-up 33 5 1 1 1 2 43

gIM, generalized inflammatory myopathy; MMM, masticatory myositis; OS, overlap syndrome (combined polymyositis and MMM); DM,
dermatomyositislike syndrome; EOM, extraocular myositis; UN, unclassified myositis; M, male; MN, castrated male; F, female; FS, spayed female.
Recovery was defined as the time from diagnosis to when dogs had shown clinical improvement but were still on medical therapy for clinical
signs of an inflammatory myopathy at the time of the report. Normal was defined as the time to resolution of clinical signs and the discontinuation
of medications for treatment of the inflammatory myopathy.
a
Mean 6 SD.

years), Pit Bull (2 6 0.0 years), and Weimaraner (2 6 1.0
years) breeds were affected at significantly younger ages (P
, .05) than other breeds in this study, and more Newfound-
lands were under 1 year of age (3/19, 15.8%) than any other
group.
Clinical Signs
Clinical signs in dogs with generalized and focal forms
of inflammatory myopathies are summarized in Table 4.
The most common clinical signs in gIMs included weak-
ness, stiff gait, dysphagia, generalized muscle atrophy, and
megaesophagus. Decreased or absent spinal reflexes (ie,
generalized lower motor signs) also were observed in 16
of 89 (17.9%) dogs with generalized weakness. Surprising-
ly, myalgia was described in only 3 dogs: 2 dogs were
diagnosed with an unclassified myositis because of a gran-
ulomatous or sarcoidlike myositis, and 1 dog was diagnosed
with T gondii infection. In Newfoundland dogs, predomi-
nant clinical signs generally were associated with laryngeal,
pharyngeal, and esophageal dysfunction. Ten dogs with
generalized muscle atrophy because of PM were reported
to have either pronounced masticatory muscle atrophy or
masticatory muscle atrophy as the initial clinical sign.
Dogs with fIMs showed clinical signs referable to the
involved muscle group, including an inability to open the
jaw, atrophy of the masticatory muscles, or exophthalmos.
Masticatory muscle atrophy alone was described in 8 dogs
(17.7%), an inability to open the jaw alone in 18 dogs
(40%), and a combined inability to open the jaw and mas-
ticatory muscle atrophy in 14 dogs with MMM (31.1%).
An inability to open the jaw also was reported as one of
the clinical findings in 7 dogs with gIM (5%) and in 1 dog
with overlap syndrome (33%). Both dogs with EOM only
demonstrated bilateral exophthalmos (100%). Three dogs
with MMM (6.6%) and 1 dog with overlap syndrome
(33%) also demonstrated bilateral exophthalmos as part of
the clinical presentation.
Generalized lower motor neuron weakness was more
common in dogs with infectious myositis compared with
dogs with other forms of a gIM. Two dogs with N caninum–
related myositis demonstrated the characteristic pelvic limb
arthrogryposis. Ten dogs with an inflammatory myopathy
were febrile on clinical examination. Six febrile dogs were
diagnosed with PM, 1 with infection by Hepatozoon amer-
icanum, 1 with neosporosis, 1 with MMM, and the other
with an unclassified myositis.
Clinicopathologic Findings
The results of clinicopathologic testing from dogs in the
different categories of inflammatory myopathy are sum-
 Canine Inflammatory Myopathies 683

Table 2. Age and clinical outcome for dogs with a generalized inflammatory myopathy: immune-mediated polymyositis
and infectious and preneoplastic myositis.a
Died/euthanized
Number Age (years) Onset (weeks) Recovery (weeks) (weeks) LTF
Immune-mediated 88 5.13 6 2.3 18.7 6 25.3 27.1 6 38.8 17.2 6 25.3 19
Range 1–10 1–156 1–104 1–104
n 88 81 54 15
Infectious 40 3.96 6 2.6 14.9 6 23.4 20 6 17.2 4.8 6 6.4 14
Toxoplasma gondii 16 5.7 6 2.5 8.5 6 7.1 14.7 6 15.9 4 6 0.0 7
Range 1.5–8 3–28 1–52
n 16 11 8 1
Neospora caninum 12 3 6 2.3 18.6 6 20.3 8.9 6 7.3 1 6 0.0 4
Range .25–8 2–52 1–24
n 12 9 7 1
Borrelia burgdorferi 7 4.4 6 2.7 5.5 6 3.8 7.5 6 2.1 9 6 9.9 3
Range 1.5–8 2–12 6–9 2–18
n 7 6 2 2
Rickettsia rickettsii 2 3.5 6 2.1 6.5 6 2.1 4 6 0.0 16 6 0.0
Range 2–5 5–8
n 2 2 1 1
Ehrlichia canis 2 3.5 6 2.1 8 6 0.0 16 6 0.0 4 6 0.0
Range 2–5
n 2 1 1 1
Hepatozoon americanum 1 1 2 6 0.0 104 6 0.0
Preneoplastic 12 6.8 6 3.2 7.8 6 7.1 N/A 37.5 6 32.8
Range 2–12 1–28 8–104
n 12 12 12

LTF, lost to follow-up. Values for recovery and normal, as previously defined, were combined in this table.
a
Mean 6 SD.

marized in Table 5. There were no significant differences Electrophysiologic Analysis

in mean white blood cell count among groups (P , .05).
The mean CK activity in dogs with gIM and overlap syn-
drome was significantly higher (P , .05) than in dogs with
MMM, dermatomyositislike syndrome, and unclassified
myopathy. CK activities were not measured in the 2 dogs
with EOM. Mean AST activity in dogs with gIM and over-
lap syndrome also was significantly higher (P , .05) than
in dogs with MMM and dermatomyositislike syndrome.
AST activities were not reported in dogs with EOM or un-
classified myositis. Mean ALT activity was significantly
lower (P , .05) in dogs with MMM and significantly high-
er (P , .05) in dogs with unclassified myositis compared
with other groups. ALT activities were not reported in dogs
with EOM and overlap syndrome. No significant differenc-
es were observed in total thyroxine concentrations among
the different groups (P , .05).
Antibodies against masticatory muscle type 2M fibers
were detected in 29 dogs with MMM (64%) and in all 3
dogs with overlap syndrome (100%). Acetylcholine recep-
tor antibody titers (n 5 49) and antinuclear antibody (n 5
28), Coombs’ (n 5 8), and rheumatoid factor (n 5 7) test
results were all negative. Antibodies against an unidentified
sarcolemmal antigen were found on histopathologic analy-
sis in 9 of 19 Newfoundlands with PM (Fig 3). Response
to edrophoniumc was negative in all dogs tested (n 5 7).
Electromyography and motor NCV findings in dogs with
inflammatory myopathies are summarized in Table 6. EMG
was performed on 63 (31.5%) dogs, and motor NCV stud-
ies were evaluated on 18 (9%) dogs. Fibrillation potentials
and positive sharp waves were identified in 50 (91%) dogs
with gIM, including those with myopathy secondary to T
gondii (5), N caninum (4), and B burgdorferi (1), and in 5
dogs with preneoplastic myositis. Similar changes also were
found in the masticatory muscles of dogs with MMM (3)
and in limb muscles of dogs with dermatomyositislike syn-
drome (2), unclassified myositis (2), and overlap syndrome
(1). Complex repetitive discharges were found in 6 dogs
with immune-mediated PM and in 2 dogs with an unclas-
sified myopathy. EMG was normal in 5 of 55 (9.1%) dogs
with gIM, including 1 with toxoplasmosis, 1 with neospo-
rosis, and 1 with preneoplastic myositis.
Mild decreases in motor NCV were found in 9 dogs with
gIM and were normal in 7 dogs with gIM and 2 dogs with
dermatomyositislike syndrome. Of the dogs with decreased
motor NCV, 2 were diagnosed with neosporosis and 1 with
toxoplasmosis. An additional dog with decreased motor
NCV had inflammatory spinal fluid analysis but was not
serologically tested for either T gondii or N caninum. One
dog with decreased motor NCV was not serologically tested
for either T gondii or N caninum but showed clinical im-
684 Evans et al

Table 3. Breed distribution of the 200 dogs with an inflammatory myopathy compared with an assumed distribution of
the general population based on the 2002 AKC registrations.
Breed gIM MMM OS DM EOM UN Total Study % AKC % Age (years)
Airedale 1 1 0.5 0.282 0.25 6 0.0
Akita 1 1 0.5 0.45 2 6 0.0
Australian Cattle Dog 1 1 0.5 0.56 8 6 0.0
Bernese Mountain Dog 1 1 0.5 0.22 8 6 0.0
Border Collie 1 1 0.5 0.16 7 6 0.0
Boxer 29 1 2 32 16 3.42 3.9 6 2.1
Briard 1 1 0.5 0.025 2 6 0.0
Brittany Spaniel 1 1 0.5 0.78 2 6 0.0
Chihuahua 1 1 0.5 3.38 4 6 0.0
Chesapeake Bay 1
Retriever 1 2 1 0.4 7 6 0.0
Cocker Spaniel 2 1 1 4 2 2.35 7.3 6 0.6
Collie 1 1 2 1 0.68 6.5 6 3.5
Welsh Corgi (Pembroke) 1 1 0.5 0.9 6 6 0.0
Dalmatian 3 2 1 6 3 0.19 5.6 6 2.7
Doberman Pinscher 2 2 4 2 1.16 4.25 6 2.2
Dachshund 1 1 2 1 4.66 4.8 6 2.3
English Bulldog 1 2 3 1.5 1.43 3.5 6 3.1
Fox Terrier 1 1 2 1 0.14 3 6 1
Golden Retriever 8 7 1 16 8 5.77 4.3 6 3.5
German Shepherd 8 3 11 5.5 4.77 5.8 6 2.6
German Shorthaired
Pointer 1 1 0.5 1.2 5 6 0.0
Greyhound 3 3 1.5 0.3 4 6 1
Jack Russell Terrier 1 1 2 1 0.14 5 6 0.0
Keeshonden 1 1 0.5 0.1 4 6 0.0
Labrador Retriever 19 5 24 12 15.3 5.8 6 2.6
Lhasa Apso 1 1 0.5 0.6 6 6 0.0
Malamute 1 1 0.5 0.25 2 6 0.0
Mastiff 1 1 2 1 0.5 3.5 6 0.7
Miniature Pinscher 1 1 0.5 1.76 8 6 0.0
Miniature Schnauzer 3 3 1.5 2.55 7.5 6 2.3
Mixed breed 8 5 13 6.5 0 5.3 6 3.6
Newfoundland 16 2 1 19 9.5 0.26 2.1 6 1.1
Old English Sheepdog 1 1 0.5 0.14 4 6 0.0
Pekingese 1 1 0.5 0.72 7 6 0.0
Pit Bull 1 1 0.5 0.16 2 6 0.0
Pomeranian 1 1 0.5 2.6 8 6 0.0
Poodle (Standard) 2 1 3 1.5 3.7 3.5 6 2.1
Pug 3 3 1.5 2.2 4.7 6 2.1
Rottweiler 5 6 11 5.5 2.7 6.9 6 3.1
Samoyed 1 1 0.5 0.15 11 6 0.0
Sharpei 1 2 3 1.5 0.5 3.6 6 2.1
Siberian Husky 1 1 0.5 1.37 9 6 0.0
Schipperke 1 1 0.5 0.157 10 6 0.0
English Springer Spaniel 1 1 0.5 0.94 9 6 0.0
Saint Bernard 1 1 0.5 0.53 5 6 0.0
Staffordshire Terrier 1 1 0.5 0.05 5 6 0.0
Terrier cross 2 2 1 0 8.5 6 0.7
Weimaraner 3 3 1.5 0.83 2 6 1
West Highland White 1 1 0.5 1.12 10 6 0.0

gIM, generalized inflammatory myopathy; MMM, masticatory myositis; OS, overlap syndrome; DM, dermatomyositislike syndrome; EOM,
extraocular myositis; UN, unclassified myositis; AKC, American Kennel Club.

provement with clindamycin alone. A final dog with pre-
neoplastic myositis secondary to lymphosarcoma also had
decreased motor NCV.
Histopathologic Characterization
Histopathologic findings of muscle biopsies from dogs in
the different categories of the inflammatory myopathies are
summarized in Table 7. The most common patterns of cel-
lular infiltrates were various combinations of lymphocytes,
histiocytes, and macrophages, with or without eosinophils.
Neutrophils rarely were found. Eosinophils were most com-
mon in dogs with an inflammatory myopathy resulting from
an infectious agent or in MMM. Twelve dogs with inflam-
matory myopathy because of T gondii (75%) and 5 dogs
 Canine Inflammatory Myopathies 685

Fig 2. Scatterplot diagram comparing the percent breed population distribution of the dogs in this investigation with an assumed breed distribution
of the general population as reported by 2002 American Kennel Club (AKC) registrations. The star and pentagon represent the Newfoundland
and Boxer breeds, respectively.

Table 4. Presenting clinical signs in 200 dogs with an inflammatory myopathy.

gIM MMM OS DM EOM UN Total
Number in study 140 45 3 3 2 7 200
Generalized clinical signsa
Generalized weakness 69 2 2 73
Stiff gait 39 1 1 1 42
Dysphagia 33 4 1 3 38
Megaesophagus 20 1 2 23
Generalized muscle atrophy 32 32
Generalized LMN signs 16 16
Dysphonia 13 1 1 15
Fever 7 1 2 10
Inability to open jaw 7 1 8
Exophthalmos 3 1 4
Focal clinical signs
Inability to open jaw only 18 18
Masticatory muscle atrophy only 8 8
Masticatory muscle atrophy and inability
to open jaw 14 14
Exophthalmos only 2 2

gIM, generalized inflammatory myopathy; MMM, masticatory myositis; OS, overlap syndrome; DM, dermatomyositislike syndrome; EOM,
extraocular myositis; UN, unclassified myositis; LMN, lower motor neuron.
a
Dogs with the generalized clinical signs had 2 or more of the listed clinical signs. Some dogs had only 1 or very focal clinical signs as listed
above.
686 Evans et al

Table 5. Summary of the clinicopathologic findings of 200 dogs with an inflammatory myopathy.a
gIM MMM OS DM EOM UN Total
Number in study 140 45 3 3 2 7 200
CK (IU/L) 6,714.9 6 8,654.5 724.2 6 687.6 5,607.3 6 5,399.1 903 6 1,127.1 NP 1,032.5 6 1,334.2 5,855.1 6 8,202.5
Range 81–55,330 100–2,595 83–10,872 106–1,700 202–3,026 81–55,330
n 96 15 3 2 4 115
AST (IU/L) 408.5 6 443.6 92.9 6 62.7 319.6 6 209.2 52 6 36.8 NP 33 342.1 6 411.5
Range 15–2,500 25–212 81–471 26–78 15–2,500
n 53 10 3 2 1 69
ALT (IU/L) 275.3 6 140.5 114.3 6 75.1 NP 176 6 0.0 NP 466.5 6 92.6 268 6 148.1
Range 32–612 71–201 131–401 32–612
n 23 3 1 2 29
WBC (310 ) 3
15.58 6 11.6 13.4 6 5.6 11.1 6 0.0 11.6 6 0.0 NP 36.2 6 49.5 15.7 6 12.6
Range 5.9–60 8.6–25.8 3–69.4 3–69.4
n 46 11 1 1 2 61
TT4 2.08 6 1.44 1.7 6 0.7 NP NP NP NP 2.05
Range 0.5–8.1 0.7–2.4 0.5–8.1
n 38 4 42
2M Ab ND ND
Positive 29 3 32
Negative 23 16 2 41
AChR Ab (negative) 43 ND 2 2 ND 2 49

gIM, generalized inflammatory myopathy; MMM, masticatory myositis; OS, overlap syndrome; DM, dermatomyositislike syndrome; EOM,
extraocular myositis; UN, unclassified myositis; CK, creatine kinase; AST, aspartate aminotransferase; ALT, alanine aminotransferase; WBC, white
blood cell count; TT4, total thyroxine concentration (RIA); 2M Ab, 2M antibody titer; AChR Ab, acetylcholine receptor antibody (myasthenia
gravis); NP, information not provided; ND, test not done.
a
Mean 6 SD.

Fig 3. Fresh frozen biopsy from the deltoid muscle of a 3-year-old female spayed Newfoundland dog with a 6-month history of dysphagia,
excessive drooling, exercise intolerance, and generalized muscle atrophy. Distinct labeling of the sarcolemma (arrow) was found after incubation
with the immunoreagent Staphylococcal protein A horseradish peroxidase indicative of bound antibodies. Bar 5 50 mm.
 Canine Inflammatory Myopathies 687

Table 6. Electromyographic (EMG) and motor nerve Table 7. Histopathologic changes in muscle biopsy spec-
conduction velocity (MNCV) studies in dogs with an in- imens of 200 dogs with an inflammatory myopathy.
flammatory myopathy.
gIM MMM OS DM EOM UN Total
gIM MMM OS DM EOM UN Total Number in study 140 45 3 3 2 7 200
Number in study 140 45 3 3 2 7 200 Cells
EMG L, M 81 35 3 1 120
Normal 5 5 L, M, E 47 10 1 1 59
FP/PS 50 3 1 2 2 58 M 5 2 3 2 12
CRD 6 2 8 Histio 6 6
PC 1 1 2
MNCV
PMN 2 1 2 4
Normal 7 2 9
Slight decrease 9 9 Distribution
EN 83 12 2 2 99
gIM, generalized inflammatory myopathy; MMM, masticatory myo- EN, PV 13 23 1 37
sitis; OS, overlap syndrome; DM, dermatomyositislike syndrome; PE 1 1 1 3
EOM, extraocular myositis; UN, unclassified myositis; FP, fibrillation EN, PE 21 1 1 23
potentials; PS, positive sharp potentials; CRD, complex repetitive dis- PF 1 1 3 5
charges. MF 7 5 1 13
Atrophy
None 9 3 2 15
with inflammatory myopathy from N caninum (41.6%) had
Mild 16 6 22
eosinophils in muscle biopsy specimens. Only 10 of 65 Moderate 40 10 2 3 (PF) 2 57
(15.3%) dogs with negative serologic titers for either T gon- Severe 27 8 3 38
dii or N caninum had eosinophils in muscle biopsy speci-
Fibrosis
mens. Eosinophils were found in 24 of 48 (50%) muscle
biopsy specimens from dogs that had not been tested for None 8 15 23
EN 56 6 1 62
either T gondii or N caninum.
PE 5 9 1 2 17
Distribution of cellular infiltrates usually was multifocal EN, PE 13 12 1 2 1 29
and most commonly endomysial with invasion of nonne- PF 3 2 5
crotic fibers or endomysial and perivascular. Perimysial and End stage 2 1 3
perifascicular distributions were also found. An endomysial
distribution of cellular infiltrates was most common in dogs gIM, generalized inflammatory myopathy; MMM, masticatory myo-
with PM, whereas a perivascular distribution was most sitis; OS, overlap syndrome; DM, dermatomyositislike syndrome;
EOM, extraocular myositis; UN, unclassified myositis; L, lympho-
common in dogs with MMM.
cytes; M, macrophages; E, eosinophils; PC, plasma cells; PMN, poly-
Atrophic fibers most typically had a round shape and morphonuclear cells (neutrophils); EN, endomysial; PV, perivascular;
involved both muscle fiber types. Occasionally, necrotic fi- PE, perimysial; PF, perifascicular; MF, multifocal.
bers or basophilic regenerating fibers were found. Muscle
fiber atrophy was most commonly moderate or severe. Per-
ifascicular atrophy was typical only of dogs with derma-
tomyositislike syndrome. An absence of fiber atrophy was of 45 dogs tested (24.4%). N caninum cysts were found in
found in 9 dogs with gIM, in 3 dogs with MMM, and in 2 muscle biopsy specimens from 2 dogs (18.2%) with sero-
dogs with unclassified myositis. logic evidence of exposure to N caninum. One dog was not
Fibrosis was present in varying degrees, having an en- tested serologically for N caninum, but N caninum cysts
domysial or perimysial distribution. Endomysial fibrosis were identified on muscle biopsy specimen evaluation.
was most common in dogs with gIM, whereas both endo- Thirty-four and 31 dogs tested negative for serologic evi-
mysial and perimysial fibroses were common in dogs with dence of exposure to T gondii and N caninum, respectively.
MMM. Complete loss of muscle fibers with replacement by Forty-eight dogs with assumed PM were not tested for se-
connective tissue (end-stage fibrosis) was found in 3 dogs, rologic evidence of either T gondii or N caninum infection.
and an absence of fibrosis was found in 23 dogs. Perifas- Serologic evidence of exposure also was found to B
cicular fibrosis was found in all 3 dogs with dermatomyo- burgdorferi (7/15, 46.6%), Ehrlichia canis (2/21, 9.5%),
sitislike syndrome. and R rickettsii (2/12, 12.5%). Reciprocal titers against an-
tigens to B burgdorferi ranged from 256 to 512. Both re-
Serology for Infectious Diseases ciprocal titers against antigens to E canis were 640, and
Results of serologic testing for various infectious diseas- reciprocal titers against antigens to R rickettsii ranged from
es are summarized in Table 8. Of the dogs tested for se- 120 to 256. H americanum cysts were found in the muscle
rologic evidence of exposure (reciprocal titers . 64) to T biopsy specimen of 1 dog. One dog also was positive for
gondii (51/200, 25.5%), 16 (31.4%) were positive. Recip- circulating antibodies to Dirofilaria immitis on routine se-
rocal titers against T gondii antigens ranged from 64 to rologic testing. Negative serologic tests for infectious
2,048. Serologic evidence of exposure to N caninum, with agents included those for Brucella canis, Babesia canis,
reciprocal titers ranging from 64 to 3,200, was found in 11 Leptospira canicola, Leptospira ictohemorrhagica, Coccid-
688 Evans et al

Table 8. Serological testing for infectious etiologies in 200 dogs with an inflammatory myopathy.
Parameter gIM MMM OS DM EOM UN Total
Number in study 140 45 3 3 2 7 200
Toxoplasma gondii
Negative 25 2 1 2 30
Positive 16 16
Neospora caninum
Negative 23 1 2 26
Positive 11a 12
Borrelia burgdorferi
Negative 5 2 7
Positive 8 7
Ehrlichia canis
Negative 15 1 1 16
Positive 2 2
Rickettsia rickettsii
Negative 11 1 1 13
Positive 2 2
Hepatozoon canis (positive) 1b 1
Dirofilaria immitis (positive) 1 1
Brucella canis (negative) 5 5
Babesia canis (negative) 5 5
Leptospirosisc (negative) 3 3
Otherd (negative) 7 7

gIM, generalized inflammatory myopathy; MMM, masticatory myositis; OS, overlap syndrome; DM, dermatomyositislike syndrome; EOM,
extraocular myositis; UN, unclassified myositis.
a
Eleven dogs had serologic evidence of exposure to N caninum. Another dog had N caninum cysts identified on muscle biopsy evaluation but
was not serologically tested for antibodies to N caninum.
b
H americanum cysts were found on muscle biopsy evaluation.
c
Serologic testing for exposure to leptospiral organisms was directed against both Leptospira canicola and Leptospira ictohemorrhagica.
d
Other serologic tests for evidence of infectious diseases included Coccidiodes immitis (2), Cryptococcus neoformans (2), Blastomyces der-
matiditis (2), and Histoplasma capsulatum (1).

ioides immitis, Cryptococcus neoformans, Blastomycoses thanized immediately after the muscle biopsy. The medical
dermatididis, and Histoplasma capsulatum. therapy employed was not reported in 86 dogs (43%).

Specific Therapies Outcome

The most common therapies used for the treatment of
inflammatory myopathy were either prednisoned alone (62),
a combination of prednisone and an antibiotic (20), or an
antibiotic alone (16). The antibiotics used alone to treat
inflammatory myopathy included clindamycine (8), cephal-
exinf (5), doxycyclineg (2), and enrofloxacinh (1). Three
dogs were treated with a combination of clindamycin and
doxycycline, and another dog was treated with a combi-
nation of gentamicini and cephalexin. One dog was treated
with a combination of trimethoprim-sulfadiazine,j clinda-
mycin, pyrimethamine,k and decolunate.l Combined pred-
nisone and clindamycin was administered to 15 dogs, and
prednisone and azathioprinem were used together in 6 dogs.
Two dogs also were treated with coenzyme Q10n and L-
carnitineo in addition to prednisone and azathioprine. Other
infrequently used drugs included pyridostigminep alone, L-
thyroxineq alone, or L-thyroxine in addition to specific ther-
apies for inflammatory myopathy. The owner of 1 dog de-
clined traditional medical treatment in favor of 14 different
homeopathic therapies. One dog died and 1 dog was eu-
Summary information regarding the outcomes of dogs
with various forms of inflammatory myopathy is shown in
Table 9. None of the dogs with MMM died or were eutha-
nized. All recovered, although many required long-term
medication to prevent relapse. Of dogs with PM, 15 died
or were euthanized, 34 were improved but still required
medication, and 20 were reportedly normal and off medi-
cation. Of dogs with infectious myositis, 5 dogs diagnosed
with T gondii and 1 dog each with N caninum, E canis,
and B burgdorferi were reported normal at the completion
of medical therapy. Six dogs with N caninum; 3 dogs with
T gondii; and 1 dog each with H americanum, R rickettsii,
and B burgdorferi were reported improved but still on med-
ication. One dog with B burgdorferi and 1 dog with T gon-
dii died, and 1 dog each with N caninum, E canis, R rick-
ettsii, and B burgdorferi were euthanized. Seven dogs with
T gondii, 4 dogs with N caninum, and 3 dogs with B burg-
dorferi were lost to follow-up. Of the dogs diagnosed with
gIM by T gondii or N caninum, 5 and 4 dogs, respectively,
were reported improved to normal after a course of clin-
 Canine Inflammatory Myopathies 689

Table 9. Outcome of 200 dogs with an inflammatory my- compared with other breeds. Megaesophagus and dysphagia
opathy. also were more common in Newfoundlands compared with
other dogs with an inflammatory myopathy.
Inflammatory Recov- Nor- Euthan-
In general, the clinical signs of focal or generalized forms
Myopathy ereda malb Died ized LTF Total
of inflammatory myopathies in the dogs of this study were
gIM 46 28 9 24 33 140 consistent with previous descriptions. Interestingly, al-
Immune-mediated 34 20 5 10 19 88 though muscle pain was reported previously in dogs with
Infectious 12 8 2 4 14 40
an inflammatory myopathy,2 myalgia was rarely reported in
Preneoplastic 2 10 12
this large group of dogs. It is possible that myalgia was
MMM 31 9 5 45 present but not detected, but the absence of myalgia is a
OS 1 1 1 3 consistent finding in humans with PM.41,42 gIMs also were
DM 1 1 1 3
present in greater number than MMM. This finding might
EOM 1 1 2
not be an accurate reflection of the frequency of these dis-
UN 1 2 2 2 7
orders because the serologic test for masticatory myositis
Total 80 40 10 27 43 200 now is available for the diagnosis of MMM and some cli-
gIM, generalized inflammatory myopathy; MMM, masticatory myo- nicians prefer to do this test alone without muscle biopsy.
sitis; OS, overlap syndrome; DM, dermatomyositislike syndrome; A previously unrecognized overlap syndrome was iden-
EOM, extraocular myositis; UN, unclassified myositis; LTF, lost to tified in 3 dogs, in which clinical signs of both MMM and
follow-up. PM were present. All 3 dogs had autoantibodies against
a
Recovery was defined when dogs had shown clinical improvement masticatory muscle type 2M fibers. In humans, an overlap
but were still on medical therapy for clinical signs of an inflammatory syndrome is defined as a severe generalized form of inflam-
myopathy at the time of the report. matory myopathy in which more than 1 immune-mediated
b
Normal was defined as a resolution of clinical signs with the dog
syndrome is present. This disorder is characterized by the
off medications for treatment of the inflammatory myopathy.
presence of PM or dermatomyositis concurrent with other
disorders of connective tissue such as scleroderma, system-
damycin alone. One dog with borreliosis was reported im- ic lupus erythematosus, and Sjögren’s syndrome.1 For the
proved after treatment with doxycycline alone. All dogs purpose of this report, overlap syndrome is defined as the
diagnosed with preneoplastic PM either died or were eu- combined diagnosis of PM and MMM. Dogs with overlap
thanized. Of the dogs with dermatomyositislike syndrome, syndrome had cellular infiltration in both limb and masti-
1 was reported recovered and off medications, 1 was re- catory muscles characteristic of PM and were positive for
ported stable while still on medications, and 1 was lost to circulating antibodies against masticatory muscle type 2M
follow-up. Of the 2 dogs with EOM, 1 was reported stable fibers characteristic of MMM. Of the 3 dogs with overlap
while still on medications and 1 was lost to follow-up. Of syndrome, 1 died, 1 was euthanized, and 1 was lost to fol-
the dogs with unclassified myopathy, 2 were reported re- low-up. These findings suggest a more severe, generalized
covered and off medications, 1 was reported stable while immune-mediated disorder in dogs with overlap syndrome,
still on medications, 2 were euthanized, and 2 were lost to as described in humans. Recently, an overlap syndrome of
follow-up. MMM and myasthenia gravis has been identified (Shelton,
unpublished observations).
On the basis of clinical and electrophysiologic exami-
Discussion
nation alone, it would be difficult to differentiate the vari-
Results of this study suggest a broader spectrum of ca- ous inflammatory myopathies. Combinations of diagnostic
nine inflammatory myopathies than previously described. tests described in this study could be useful in reaching a
Although several breeds of dogs were affected, Boxers and diagnosis. Clinically, masticatory muscle atrophy and an
Newfoundlands were overrepresented. Of 32 Boxers ini- inability to open the jaw were most common in MMM but
tially diagnosed with gIM, 6 were diagnosed with lympho- also were found in several cases of gIM with subclinical
ma several months later. An anaplastic round cell tumor and limb muscle involvement. Masticatory muscle atrophy
a plasmacytoma also were later diagnosed in 2 other Boxers might be a sequela of chronic corticosteroid therapy re-
after the onset of gIM. At the time of diagnosis of the gardless of the underlying disease process.43 Muscle biopsy
inflammatory myopathy, no evidence of neoplastic cells and serum antibody titers against masticatory muscle type
was found in the biopsy sections, whereas at the time of 2M fibers should differentiate MMM and PM, but these
diagnosis of neoplasia, neoplastic cells were observed in antibodies can be present in overlap syndrome.
the muscle biopsies. This finding suggests that inflamma- Similarly, an etiology for the inflammatory myopathies
tory myopathy might be a preneoplastic syndrome in this would be difficult to determine from histopathology alone.
breed. Neoplasia also developed within 12 months of initial An endomysial and perivascular distribution of cellular in-
diagnosis in 4 other breeds of dogs. Breed-associated PM filtrates and endomysial and perimysial fibrosis were most
was identified in the Newfoundland dogs. Unlike the other common in dogs with MMM, whereas an endomysial dis-
breeds, these dogs had circulating autoantibodies against an tribution of cellular infiltrates and endomysial fibrosis were
unidentified sarcolemmal antigen supporting a humoral im- most common to gIM syndromes. Although lymphocytes
mune component. With the exception of a few sporadic and macrophages were common to all of the inflammatory
cases of inflammatory myopathy in other breeds, New- myopathies, the presence of eosinophils suggested infec-
foundlands with PM tended to be affected at a younger age tious myositis. Eosinophils also were found in approxi-
690 Evans et al
mately 30% of masticatory muscle biopsies from dogs with
MMM. Parasitic cysts in muscle biopsies also would sup-
port an infectious disorder. In a recent immunohistochem-
ical study evaluating phenotypes of cellular infiltrates in
dogs with an inflammatory myopathy, it was similarly dif-
ficult to classify the gIMs on the basis of histopathology
alone.27 In that study, populations of dendritic cells in dogs
with infectious myositis were markedly increased over T
cells compared with that observed in dogs with PM, but
inflammatory myopathies resulting from immune-mediated
and preneoplastic disorders could not be differentiated.
Both MMM and EOM can present clinically with ex-
ophthalmos from inflammation of the temporalis and pter-
ygoid muscles in MMM and the extraocular muscles in
EOM.23,24 The 2M antibody titer should differentiate these
2 disorders. Typical skin lesions in dogs with dermatomy-
ositis should differentiate this disorder from other gIMs. In
addition, the distribution of the cellular infiltration, muscle
fiber atrophy, and fibrosis in dogs with dermatomyositislike
syndrome was perifascicular.
The presence of circulating antibodies to infectious
agents such as T gondii or N caninum is suggestive of in-
fectious myositis, but definitive diagnosis can only be made
by identification of organisms in muscle biopsy specimens.
Although an increased macrophage or histiocytic cell pop-
ulation might be indicative of an infectious etiology,27 min-
imal histologic differences can be identified in dogs with
PM and in those with concurrent antibodies against infec-
tious agents; consequently, appropriate antimicrobial ther-
apy is warranted. The clinical response of some of these
dogs to antimicrobial therapy alone supports this recom-
mendation. If the association between eosinophils in the
muscle biopsy specimens and infectious disorders is accu-
rate, infectious myositis, especially from T gondii and N
caninum, could be more common than previously believed.
Further investigation of this association is warranted, and
we recommend serologically testing all dogs diagnosed
with gIM for both T gondii and N caninum as part of the
minimum database.
The pathologic changes in 7 dogs did not fall into the
specific classification groups. Dogs in this category had
generalized clinical signs and were negative for 2M anti-
bodies and for antibodies against infectious agents. The his-
tologic characterization was that of collagen–vascular dis-
orders, granulomatous myositis, and sarcoidlike myopathy,
as described in humans. Further investigations are needed
to more accurately classify these disorders.
Over the long term, with appropriate therapy, dogs with
MMM tended to improve, as did dogs with gIM, although
residual muscle atrophy, particularly in the masticatory
muscles, or reduced muscle function remained in some
dogs. Dogs with inflammatory myopathy because of pre-
sumed infectious etiology also improved, provided an ac-
curate diagnosis was made and appropriate antimicrobial
therapy employed. Although follow-up was not available
on a large number of dogs, preneoplastic myositis generally
carried a poor prognosis.
On the basis of the results of this study, more than 1
diagnostic modality is required to confirm an etiology for
inflammatory myopathy. Muscle biopsy is critical for the
identification of inflammatory myopathies in general and
can determine an etiology in some cases. A combination of
clinical signs, serologic testing for autoantibodies and in-
fectious agents, and immunophenotyping of cellular infil-
trates in muscle biopsy specimens might be required to de-
termine a specific etiology. With the exception of the pre-
neoplastic syndromes, most inflammatory myopathies are
treatable if diagnosed early and treated appropriately.
Footnotes
a
2M antibody titer, Comparative Neuromuscular Laboratory, Univer-
sity of California, San Diego, La Jolla, CA
b
Acetylcholine receptor antibody titer, Comparative Neuromuscular
Laboratory, University of California, San Diego, La Jolla, CA
c
Edrophonium, Tensilon, Anaquest, Liberty Corner, NJ
d
Prednisone, Deltasone, Upjohn Company, Kalamazoo, MI
e
Clindamycin, Antirobe, Upjohn Company, Kalamazoo, MI
f
Cephalexin, Keflex, Dista, Indianapolis, IN
g
Doxycycline, Vibramycin, Pfizer, Inc, New York, NY
h
Enrofloxacin, Baytril, Miles, Inc, Shawnee, KS
i
Gentamicin, Gentocin, Schering-Plough Animal Health, Kenil-
worth, NJ
j
Trimethoprim/Sulfadiazine, Tribrissen, Mallinckrodt Veterinary, Inc,
Mundelein, IL
k
Pyrimethamine, Daraprim, Burroughs Wellcome, Research Triangle
Park, NC
l
Decoquinate, Deccox, Alpharma Inc, Fort Lee, NJ
m
Azathiaprine, Imuran, Burroughs Wellcome, Research Triangle
Park, NC
n
Coenzyme Q10, CoMal Q10, Nutramax Laboratories, Edge-
wood, MD
o
Levocarnatine, Carnitor, Sigma Tau Pharmaceuticals, Inc, Gaithers-
burg, MD
p
Pyridostigmine, Mestinon, Roche Merieux, Inc, Athens, GA
q
Levothyroxine, Soloxine, Daniels Pharmaceuticals, Inc, St. Peters-
burg, FL
Acknowledgments
The authors thank Norma Prades for excellent technical
assistance. Funding for this study was provided by a grant
from the Muscular Dystrophy Association (GDS)
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