Non-exertional myopathies (Proceedings)


Non-exertional myopathies (Proceedings)

Nov 01, 2010

Characterized by clinical and laboratory findings of muscle damage not associated with exercise. Includes inflammatory, nutritional, toxic, traumatic, metabolic, congenital, immune mediated and idiopathic causes of muscle disease.

Inflammatory myopathies: Myopathy related to infectious agents or immune mediated damage.

Clostridial myositis:
     • Rapid, progressive muscle necrosis associated with multiplication of Clostridium within muscle and a systemic inflammatory response. Also called blackleg, gas gangrene and malignant edema.
     • Affects horses, humans, ruminants and other species.

Infection may occur via direct inoculation (injection site or a wound) or from spores present in the muscle tissue and proliferate in response to triggering factors such as trauma.
     • Clinical signs: In horses: usually arises at IM injection sites (80% of cases), but can develop in regions of muscle trauma and in open wounds. Clinical signs arise within 48 hours. Firm, hot, swollen and painful area often with crepitance. Tachycardia, tachypnea, fever and lameness are common. Complications include IMHA, coagulopathies and laminitis. Clostridium septicum and Clostridium perfringens are the most frequently isolated organisms in horses.
     • Lab findings: elevated CK and AST (usually mild), CBC consistent with toxemia and inflammation.
     • Diagnosis is based on clinical signs, ultrasonography (fluid pockets, gas production, edema), cytology of aspirated fluid (large gram positive rods) and the growth of Clostridia on anaerobic culture.
     • Treatment: Penicillin and/or metronidazole. Surgical debridement and wound flushing. Initial antibiotic treatment is aggressive (penicillin 44 000 IU/kg every 2 to 4 hours until the animal is stable)
     • Adjunct therapy: anti- inflammatory drugs, IV fluids, analgesia, hydrotherapy, topical wound therapy, fly control.
     • High mortality rate (~ 68%), so early and aggressive therapy is critical. Infections with Cl. septicum are associated higher mortality rate than Cl. perfringens (85% vs. 25%). Cl. sordelli invariably fatal.
     • Prevention: no licensed equine vaccine.

Viral myositis:
     • Herd outbreaks of equine influenza A2 have been associated with a small % of horses developing severe myositis. Affected horses presented with fever, depression, dehydration and stiffness which progressed to renal failure and death. Virus was isolated from the lungs but not muscle tissue.
     • EHV 1 has also been associated with signs of muscle stiffness in some herd outbreaks.

Sarcocystis myositis:
     • Cysts of the parasite Sarcocystis are commonly found on microsopic examination of cardiac, esophageal and skeletal muscle of horses.
     • Carnivores are definitive hosts, herbivores are intermediate hosts and usually exposed through contamination of feed sources with fecal material from definitive hosts.
     • Infection is usually asymptomatic.
     • Heavily infected horses may display low grade fever, malaise, stiffness, muscle atrophy and mild elevations in CK with a large number of sporocysts on muscle biopsy with associated neutrophilic or eosinophilic inflammation. Firm lumps may be palpable within the muscle. Affected horses can be treated with anti-inflammatory drugs, anti-protozoal drugs (TMS + pyramethamine, or ponazuril) and potentially corticosteroids if problems persist over time.