Canine inflammatory myopathies: a clinicopathologic review of 200 cases

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 generalized 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 = .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 (flM)--including masticatory muscle and extraocular 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.     

Immunopathogenic pathways in canine inflammatory myopathies resemble human myositis

Progress in the treatment of inflammatory myopathies is impeded by the lack of suitable animal models. Inflammatory myopathies occur spontaneously in the dog, are a heterogeneous group of disorders, and are more common than in humans. Clinical signs of weakness and muscle atrophy are reliably present, and there are histological and immunohistological similarities to forms of human myositis. In this study, microarray technology followed by quantitative real-time PCR and immunohistochemistry on muscle biopsy sections was used to investigate gene expression in cases of canine inflammatory myopathies. Several genes involved with innate and adaptive immunity were highly upregulated including those that participate in macrophage and dendritic cell activation and migration, and antigen processing and presentation. Other genes including those that participate in B cell growth, development, migration and activation, immunoglobulin genes, genes in pro-inflammatory and anti-inflammatory pathways, and genes involved with tissue remodeling were upregulated. In previous reports utilizing microarray technology in human myositis, there was activation of similar pathways involved in the immune response. This study strengthens the argument that forms of canine myositis may be important animal models of human myositis and suggests useful biomarkers for therapeutic response using the dog in pre-clinical trials.     

Haycocknema-like nematodes in muscle fibres of a horse

A 14-year-old horse (imported to Switzerland from Ireland 8 years earlier) showed signs of chewing muscle atrophy. A severe chronic myositis, caused by numerous immature and mature female nematodes, was diagnosed in muscle samples obtained by biopsy and subsequently at necropsy. Most of the nematodes had invaded muscle fibres of the masseter, root of the tongue and anterior breast, only a few were found in the intermuscular interstitium. Isolated nematodes and parasite sections were clearly different from muscle larvae of Trichinella spp. but showed morphological similarities to Haycocknema perplexum, a nematode species (order Enoplida, family Robertdollfusidae) recently found in the musculature of a human patient in Australia. However, our material did not allow the precise identification of the nematode genus nor the unequivocal differentiation from Halicephalobus gingivalis. This species infects horses and humans and can cause severe granuloma formation in muscles and many other organ systems, but has never been observed to invade individual muscle fibres. Our findings show that nematodes of another genus than Trichinella may invade muscle fibres of the horse and cause myositis. These nematodes are provisionally regarded as Haycocknema-like.     

Progressive ossifying myositis in a cat

Progressive ossifying myositis was diagnosed in a 2-year-old female cat. Clinical signs consisted of cervical pruritus, a stiff gait involving the forelimbs, and decreased range of motion of the scapulohumeral joints. The signs progressed over a 2-month period to involve the hindlimbs and coxofemoral joints. The primary cause of this disease is unknown and treatment is palliative. Treatment with diphosphonate disodium etidronate was unsuccessful in controlling the clinical signs in this case.     

A myopathy of sheep associated with sarcocystis infection and monensin administration

An outbreak of muscle disease affected approximately 20 of 600 ewes in spring 1987 in south-east Scotland. The clinical signs were a flaccid paralysis of the hind limbs and in severe cases collapse. Serum creatine kinase and aspartate aminotransferase activities were increased. Clinically affected sheep had a mean reciprocal serum antibody titre in a sarcocystis immunofluorescence antibody test of 557 whereas 22 sheep from the same flock, sampled one year earlier, showed a mean reciprocal titre of only 51. Histologically a heavy infestation of sarcocysts, myodegeneration and a non-suppurative myositis centred on degenerating sarcocysts were observed in a wide range of skeletal muscles and myocardium from four affected sheep. Monensin sodium had been inadvertently included in the protein pellet used in the feed for one week before the onset of the disease.     

Elevated IgG antibody to Sarcocystis cruzi associated with eosinophilic myositis in cattle

Blood sera, skeletal muscle, and cardiac muscle from 24 bovine carcasses condemned for eosinophilic myositis by US Department of Agriculture meat inspection veterinarians were compared with similar specimens from 35 random carcasses passed for human consumption. Fluorescence values determined by using a fluorometric immunoassay system were used to measure the specific antibodies to Sarcocystis cruzi. The values were significantly elevated in carcasses condemned for eosinophilic myositis as compared to carcasses passed for human consumption. The elevated fluorescence values appeared to be more than coincidental, suggesting that S. cruzi may be a causative agent of eosinophilic myositis. Microscopic examination of affected muscle revealed lesions typical of eosinophilic myositis. Lesions were characterized by extensive multifocal areas of myofiber hyaline degeneration, necrosis with sarcoplasmic fragmentation, mineralization of occasional myofibers, and atrophy of fibers with varied stages of fibrosis. Inflammatory cell exudates were predominantly eosinophils, with some macrophages and lymphocytes, and extravasated erythrocytes within, and adjacent to, affected myofibers. Affected muscles contained more S. cruzi than unaffected muscle from passed carcasses. However, a distinct cause and effect relationship could not be determined between the parasite and the presence of eosinophilic myositis.     

Treatment of canine pediatric Neospora caninum myositis following immunohistochemical identification of tachyzoites in muscle biopsies

A 7-week-old Irish wolfhound was evaluated for an abnormal hind limb gait. Quadriceps muscle atrophy was pronounced and patellar reflexes were absent bilaterally. Neospora caninum myositis was diagnosed by histopathologic and serologic examination and immunohistochemical staining of muscle. Substantial clinical improvement was noted after 18 weeks of treatment with clindamycin.     

Malignant edema in horses

Malignant edema (clostridial myositis) was diagnosed in 9 horses with signs of illness that included fever, depression, painful muscular swellings, and toxemia. The infection followed intramuscular injections in 8 horses and developed in a puncture wound in 1 horse. Treatment consisted of surgical fenestration of the involved muscle, high doses of penicillin, nonsteroidal anti-inflammatory agents and analgesics, and supportive fluid therapy. Five horses recovered and 4 died. Those that died had advanced signs of the disease at admission.     

Suspected immune-mediated myositis in horses

BACKGROUND: Although immune-mediated myositis (IMM) is commonly reported in other species, this condition is poorly described in horses. HYPOTHESIS: IMM occurs in horses. ANIMALS: Thirty-seven horses with suspected IMM were included in the study. METHODS: The database of the Neuromuscular Diagnostic Laboratory was reviewed to identify 37 horses with muscle biopsies characterized by lymphocytic infiltrates. A retrospective standardized questionnaire regarding clinical signs and response to treatment was answered by horse owners. RESULTS: Horses with suspected IMM were predominantly of Quarter Horse bloodlines (33/37 horses) and primarily either < or =8 years or > or =17 years of age. Clinical signs included rapid atrophy, particularly of the epaxial and gluteal muscles, depression, and stiffness. Creatine kinase (CK) activity (mean 9746; range 260-139,183 U/L: reference range 119-287 U/L) and aspartate transaminase (AST) activity (mean 2880; range 350-9009 U/L: reference range 138-409 U/L) were high. Exposure to horses with infectious respiratory disease occurred in 39% (9/23) of horses before clinical signs and 47% (9/19) had recurrence of atrophy. Variation in dosage and time elapsed before administration of corticosteroids confounded assessment of treatment efficacy. Macrophages and CD4+ T lymphocytes were the prominent mononuclear cellular infiltrates with lesser numbers of CD8+ cells and small clusters of B lymphocytes in some samples. Myofibers did not stain for equine immunoglobulin G (IgG). CONCLUSIONS AND CLINICAL IMPORTANCE: IMM appears to be a distinct cause of rapid muscle atrophy, particularly in Quarter Horses that may be amenable to treatment with corticosteroids. Diagnosis is best achieved by identifying lymphocytic infiltrates in atrophied muscles.     

Unusual biphasic disease in domestic pigeons (Columba livia f. domestica) following experimental infection with Sarcocystis calchasi

A novel Sarcocystis species has recently been reported in the domestic pigeon (Columba livia f. domestica) as intermediate host, causing severe central nervous signs similar to Paramyxovirus-1 or Salmonella Typhimurium var. cop. infection. Transmission of the parasite via the northern goshawk (Accipiter gentilis) as definitive host has been established. Experimental infection of domestic pigeons with sporocysts excreted by experimentally infected northern goshawks reproduced the natural infection in the pigeon, proving the causative role of the parasite in the disease. Here, we describe in greater detail the course of the fulminant biphasic disease depending on the infectious dose. Pigeons infected with 10(3) or 10(4) sporocysts showed clinical signs of polyuria and apathy around 10-11 days postinfection (dpi) and sudden neurological signs 51-57 dpi as a second phase of disease. Pigeons infected with higher doses died within 7-12 dpi, also showing polyuria and apathy but without nervous signs. At necropsy, livers and spleens had multifocal necroses and infestations with parasitic stages, namely, schizonts. Moreover, lesions and schizonts were also found in the lung, bone marrow, and next to blood vessels in the connective tissue of various organs. Pigeons infected with 102 sporocysts remained symptomless until 58-65 dpi, when sudden central nervous signs occurred. Major histopathologic findings of pigeons with neurological signs were encephalitis and myositis of virtually every skeletal muscle with high infestations of sarcocysts. Only mild myocarditis and very few cysts were found in the heart muscles. Importantly, a sentinel pigeon developed identical lesions when compared to those of low-dose infected pigeons, suggesting a risk of mechanical transmission of sporocysts from freshly infected to uninfected pigeons in a flock. By contrast, chickens failed to develop any clinical signs or pathologic lesions in the same experiment. The findings further characterize the new highly pathogenic disease in domestic pigeons, which clinically mimics paramyxovirosis and salmonellosis in both phases of the disease and exclude chickens as further intermediate host species.     

Computed tomographic appearance of masticatory myositis in dogs: 7 cases (1999-2006)

OBJECTIVE: To document computed tomography (CT) features in dogs with masticatory myositis. DESIGN: Retrospective case series. ANIMALS: 7 dogs with an immunologic diagnosis of masticatory myositis and an absence of clinical abnormalities of any skeletal muscles other than the masticatory muscles. PROCEDURES: History; clinical, hematologic, biochemical, immunologic, cytologic, and histologic findings; and pre- and postcontrast CT imaging features of masticatory muscles and head and neck lymph nodes were extracted from medical records. RESULTS: On CT images, changes in size (atrophy or swelling) were common for all masticatory muscles except the digastricus muscles, which were involved only in 1 dog. Pre-contrast attenuation changes, most often hypoattenuation with varied distribution patterns, were seen in masticatory muscles of 4 dogs. Contrast enhancement with a predominantly inhomogeneous distribution pattern was seen in the temporalis, masseter, and pterygoid muscles of all dogs. Head and neck lymph nodes were enlarged in all but 1 dog and had contrast enhancement with predominantly central or homogeneous distribution patterns. Muscle biopsy was performed in 6 dogs, with biopsy specimens obtained from areas that had the most obvious contrast enhancement on CT images. For all 6 dogs, biopsy specimens had histologic features indicative of masticatory myositis. CONCLUSIONS AND CLINICAL RELEVANCE: Results suggested that CT may be a useful adjunct in the diagnosis of masticatory myositis in dogs, including selection of sites for diagnostic muscle biopsy.     

Post anesthetic myositis in the horse associated with in vitro malignant hyperthermia susceptibility

Four horses with clinical and biochemical evidence of post-operative myositis following halothane anesthesia and characterized by well localized (lumbar) to generalized rigidity and pain are described. Response to Dantrolene Sodium therapy at 4 mg/kg per os was dependent upon rapidity of administration following onset. In vitro exposure of muscle to halothane and caffeine revealed increased sensitivity when compared to control horses.     

Fatal necrotising fasciitis and myositis in a cat associated with Streptococcus canis

Necrotising fasciitis and necrotising myositis are rare but serious life threatening conditions reported mainly in human beings and dogs. Most cases to date have been caused by beta-haemolytic streptococci of Lancefield groups A, B, C or G. Necrotising fasciitis has been reported only twice in cats and necrotising myositis has never been described. This paper describes a fatal case of necrotising fasciitis and myositis with pneumonia and septicaemia in a nine-year-old cat. The cat had been undergoing treatment for a suspected tear of the cranial cruciate ligament, but on the seventh day of treatment it suddenly deteriorated and died. On postmortem examination, there was an area of hair loss from its left hindlimb and discoloration of the underlying fascia and biceps femoris muscle. Severe necrotising fasciitis and myositis, with numerous intralesional Gram-positive coccoid bacteria, was diagnosed histologically. Other findings included necrotising pneumonia, pleuritis, focal encephalitis, myocarditis and nephritis. Culture of the affected tissues yielded a pure, heavy growth of Streptococcus canis.     

Toxic Myopathy in a Dog Associated with the Presence of Monensin in Dry Food

This report describes a case of toxic myopathy in a two year old sheltie dog with clinical signs of profound weakness, myoglobinuria, and muscle enzyme elevations. The clinical signs were likely related to the accidental inclusion of monensin sodium in the dog's food. This food was prepared by a small feed milling company that also prepares cattle and chicken rations. A change of dog food resulted in remission of the clinical signs.     

An outbreak of sarcocystosis in a cattle herd.

In a cattle herd, 3 steers had anorexia and variable emaciation; 1 showed additional muscle stiffness, pyrexia, became recumbent and was killed in extremis. Gross changes in tissue specimens from this steer included grey-white foci in the skeletal muscle and a thickened, fibrous pleura. By histology interstitial pneumonia, myocarditis and necrotizing myositis were seen. There were wide-spread vascular lesions with endothelial damage, thrombosis and periarterial infiltrations. Sarcocystis-like schizonts were found in several organs, and different stages of thin-walled sarcocysts were seen in the myocardium. Examination of organs of 6 other steers in the same herd slaughtered 2 months later showed myocarditis, myositis, interstitial pneumonia and occasional vascular occlusions. There were a few schizonts in the spleen and lungs, and thin-walled sarcocysts were seen in the myocardium and skeletal muscle. It is concluded that development of vascular lesions probably represents an important step in the pathogenesis of sarcocystosis.     

Kinematic characteristics of myositis ossificans of the semimembranosus muscle in a dog

A 6-year-old Doberman pinscher dog was presented with myositis ossificans of the semimembranosus muscle. Linear, temporal, and angular kinematic patterns were recorded and compared with those of sound dogs of the same breed. The results indicate that the specific gait compensations occurring with this disease may aid in the diagnosis of myositis ossificans of the caudal thigh muscles.     

Ultrastructural and transmission evidence of Sarcocystis cruzi associated with eosinophilic myositis in cattle.

Skeletal muscle, diaphragm, tongue, esophagus and heart of beef carcasses that were condemned for eosinophilic myositis and those that were unaffected were collected at an abattoir in Colorado and studied to determine the involvement of Sarcocystis spp. All affected carcasses contained similar granulomatous lesions with adjacent infiltrations of leukocytes. Intact or fragments of sarcocysts were found within 32 of 363 granulomas, and whole sarcocysts were present in nearby unaffected muscle cells. Light and electron microscopic examinations revealed that sarcocysts, affected or unaffected by cellular response in condemned carcasses, as well as those found in unaffected carcasses, were consistent with those of S. cruzi. Transmission experiments confirmed that S. cruzi were present in all carcasses, and that dogs, but not cats, were the definitive hosts. The results of pepsin-HCl digestion assays showed that unaffected carcasses that were approved for human consumption generally contained more infective parasites than carcasses that were condemned for eosinophilic myositis. This study provides evidence to support the suggestion that dogs, rather than cats, and unaffected rather than eosinophilic myositis-affected carcasses, have greater potential for contributing to the perpetuation of eosinophilic myositis in the cattle industry.     

Congenital myasthenia gravis in Smooth-Haired Miniature Dachshund dogs

Three 8-week-old Miniature Smooth Haired Dachshund littermates were diagnosed with myasthenia gravis based on clinical signs, results of electrophysiological testing, and response to the short-acting anticholinesterase drug, edrophonium chloride. Congenital myasthenia gravis was confirmed by the demonstration of decreased acetylcholine-receptor density in external intercostal muscle in the absence of demonstrable serum antiacetylcholine receptor antibody or antibodies complexed to acetylcholine receptors in muscle biopsy samples. Unlike most previously reported cases of congenital myasthenia gravis that are relentlessly progressive, clinical signs resolved spontaneously by 6 months of age.     

Locked jaw syndrome in dogs and cats: 37 cases (1998-2005)

A consecutive series of cases of dogs and cats with locked jaw syndrome (inability to open or close the mouth) are reported in this study. Dogs were significantly overrepresented (84.0%) and adult dogs were more frequently affected (81.0%). Temporomandibular joint ankylosis due to fracture was the most common cause (54.0%) of locked jaw syndrome. Additional potential causes of locked jaw syndrome are masticatory muscle myositis, neoplasia, trigeminal nerve paralysis and central neurological lesions, temporomandibular joint luxation and dysplasia, osteoarthritis, retrobulbar abscess, tetanus, and severe ear disease. Treatment of locked jaw is directed towards the primary cause. It is important to treat the tonic spasm in order to minimize periarticular fibrosis. Surgical intervention is recommended for temporomandibular joint ankylosis. Masticatory muscle myositis treatment is initiated by gradually opening the mouth, with medical treatment based on immunosuppressive therapy. Fracture and masticatory muscle myositis are associated with a relatively good prognosis in regard to short-term outcome as compared to animals with central neurologic lesions or osteosarcoma which have a poor prognosis.     

Trypanosomiasis and laryngeal paralysis in a dog

Laryngeal paralysis and trypanosomiasis were diagnosed in a 12-year-old Labrador Retriever. Bilateral vocal fold resection and partial excision of the left aryepiglottic fold resolved the dog's respiratory difficulty. Trypomastigotes resembling Trypanosoma cruzi were seen in blood smears during hospitalization. In spite of treatment with nifurtimox and dexamethasone, the dog died. Histologic examination of tissues did not reveal amastigotes of T cruzi or granulomatous myositis previously described in canine trypanosomiasis reported from North America. The lack of granulomatous myositis and amastigotes in muscle is unusual and suggests a strain variation in the behavior of T cruzi.