Inflammatory Myopathies

Inflammatory Myopathies

Inflamitory Myopathies 
Immune-Mediated Myositis

Inflamatory Myopathies: 

Rhabdomyolysis in conjunction with S. Equi infection 

Severe Rhabdomyolysis 
Severe, fatal rhabdomyolysis has been seen in association with Streptococcus equi infections.
Clinical signs: febrile, stiff, reluctant to move, recumbency, CK > 50,000 U/L
The reason for the massive rhabdomyolysis is not completely clear, but a toxic shock-like syndrome may occur in some of these horses.

Vascular Infarction 
Rarely, some horses vaccinated for, or exposed to, S. equi within the last month develop high serum CK activity (>30,000 U/L), acute, firm swellings within muscle and under the skin, marked lameness colic signs. The elevations in serum CK are much greater that the frequent mild elevations observed in conjunction with purpura hemorrhagica.
Clinical signs: firm swellings within muscle and under the skin, lameness, limb edema, and acute colic
Diagnostics: Leukocytosis, hyperfibrinogenemia, hypoprotenemia and elevated serum CK, and AST are consistently present. Ultrasonography of swollen muscles reveals hypoechoic areas of hemorrhage. Infarctions of skeletal muscle, subcutaneous tissue, focal areas of the gastrointestinal tract and lungs resulting from a severe vasculopathy have been identified on post-mortem in these cases.
Treatment: Without aggressive corticosteroid therapy horses usually die from intestinal infarction. Treatment with IV penicillin and IV dexamethasone (0.12-0.2 mg/kg) daily for 10 days followed by tapering doses of prednisolone at an initial dose of 1-2 mg/kg have been successful in a few cases.

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Immune-mediated myositis: 

Another common form of immune-mediated myositis in Quarter Horses and related breeds appears to be related to exposure to streptococcal organisms or to other infections. The primary clinical manifestation of this myopathy is rapid atrophy of lumbar and gluteal muscles. If left untreated horses may lose half of their muscle mass within 5 days and become weak.

Clinical signs: inappetence, rapid atrophy of epaxial and gluteal muscles

Diagnostics: CBC and serum chemistry is often normal apart from modest persistent elevations in serum CK and AST (1000-40,000 IU/L). Muscle biopsies are key to a diagnosis. A diagnosis can often be made on several trucut samples of the gluteal and epaxial muscles fixed in formalin. The characteristic features of muscle biopsies taken during the first week of atrophy are; a lymphocytic vasculitis, atrophy of type 2 fibers, intense lysosomal staining with an acid phosphatase stain, occasional lymphocytic myofiber infiltration as well as waves of rhabdomyolysis and regeneration. Some untreated cases may show significant fibrosis around blood vessels and a few cases have progressed to involve systemic dystrophic calcification resulting in signs of dyspnea and severe depression.

Patholophysiology: This appears to be a cell mediated immune response to antigens in the muscles possibly as a result of antigenic similarities between the M protein of some streptococcal organisms and the contractile protein myosin.

Treatment: Corticosteroid therapy such as dexamethasone (0.05 mg/kg) for 3 days, followed by prednisolone (1 mg/kg for 7 to 10 days) tapered by 100 mg/week over 1 month, is usually successful in halting the atrophy and restoring appetite. Concurrent antibiotic therapy is recommended if a leukocytosis, hyperfibrinogenemia or lymphadenopathy is present. Muscle mass will gradually return over 2-3 months. Some horses may show signs of recrudescence of the syndrome upon re-exposure to respiratory infections.