Infectious Myopathies in Horses

Necrosis of skeletal and cardiac muscle may occur in association with viral diseases such as equine influenza and equine infectious anemia. In most situations, viral-induced muscle damage represents a component of systemic multiple organ system involvement. Equine influenza 2 has been found to cause severe rhabdomyolysis, and equine herpesvirus 1 has been reported to induce primary muscle stiffness and clinical signs resembling exertional rhabdomyolysis.

Cysts of the sporozoan parasite Sarcocystis were present in 88.9% of esophageal muscles from horses >8 years of age in an abattoir study.1 In another study, sarcocysts were found in 10 of 164 (6%) gluteal muscle biopsies from healthy Quarter Horses.2 Occasionally, heavy infestations occur via contamination of feed with canine feces, resulting in clinical signs of fever, anorexia, stiffness, weight loss, muscle fasciculations, atrophy, and weakness. Diagnosis of sarcocystosis requires history, clinical signs, laboratory evaluation, and the demonstration of an inflammatory reaction to immature cysts in muscle biopsies. Treatment includes NSAIDs and drugs such as trimethoprim sulfa and pyrimethamine or ponazuril. (Also see Sarcocystosis.)

Horses that acquire Anaplasma phagocytophilum from tick infestations can rarely develop clinical signs of severe muscle stiffness in addition to fever, malaise, and limb edema. Hematologic findings include anemia, thrombocytopenia, neutropenia, morula visible in granulocytes, and marked increases in serum CK and AST activities. A diagnosis is confirmed by PCR assay testing of blood for A phagocytophilum. A direct toxic effect of A phagocytophilum on muscle cells is postulated; however, many Quarter Horses with A phagocytophilum and rhabdomyolysis have tested positive for the MYH1 mutation causing myosin heavy chain myopathy. Treatment should include oxytetracycline (7 to 10 mg/kg, IV slowly, every 24 hours for 7 to 10 days) and supportive care.

A variety of clostridial bacteria can sporulate at the site of an injection or deep wound, causing focal muscle swelling and systemic toxemia in horses. Clostridium septicum, C chauvoei, C sporogenes, and mixed infections are associated with a high fatality rate; C perfringens type A has a mortality rate of 20% with early and aggressive treatment. Clostridial spores may lie dormant in skeletal muscle, or spore deposition directly into the tissue may occur in association with penetration. If suitable necrotic conditions exist, the spores convert to the vegetative form, releasing exotoxins.

Within 48 hours, horses show lethargy, fever, toxemia, tachypnea, and swelling and variable crepitus at the injection site. Tremors, ataxia, dyspnea, recumbency, coma, and death may occur in the next 12–24 hours. Myocardial damage occurs in some horses. Hematologic and serum biochemical analyses usually reflect a generalized state of debilitation and toxemia (eg, hemoconcentration and a stress or toxic leukogram may be present). Serum CK and AST activities are usually moderately increased; however, they often do not reflect the toxic effects of clostridial myonecrosis.

Ultrasonographic evaluation of swollen areas may reveal fluid and characteristic hyperechoic gas accumulation. Aspirates of affected tissues examined via direct smears or fluorescent antibody staining should show characteristic rod-shaped bacteria. Anaerobic bacterial culture of freshly acquired samples may also be of value. Cut tissue from the affected area may reveal abundant serosanguineous fluid with an odor of rancid butter. At postmortem examination, swelling, crepitus, and autolysis are rapid, and hemorrhagic fluid is often observed discharging from body orifices.

Wound fenestration and aggressive surgical debridement over the entire affected area is required for successful treatment. Additional treatment includes high doses of potassium penicillin (30,000 to 60,000 U/kg, IV, every 2–4 hours until the horse is stable [1 to 5 days]), combined with or followed by metronidazole (20 to 25 mg/kg, PO, every 6 hours for 20 days) along with supportive fluid therapy and anti-inflammatory agents. Extensive skin sloughing over the affected area is common in surviving horses.

Staphylococcus aureus, Streptococcus equi, and Corynebacterium pseudotuberculosis are common causes of skeletal muscle abscesses, which develop after penetrating injuries or by hematogenous or local spread of infection. Initially, there is an ill-defined cellulitis, which may heal or progress to a well-defined abscess. An abscess may heal, expand, or fistulate, usually to the skin surface, with potential for a chronic granuloma with intermittent discharge. Prognosis is usually good for superficial abscesses. Deep abscesses are more difficult to manage successfully.

The effect of an abscess on the horse’s gait depends on its location and can vary from mild stiffness to severe lameness. Ultrasonographic evaluation and culture of aspirated fluid are the best means of diagnosis in superficial sites. Abscesses lying deep within muscles can be difficult to diagnose. Clinicopathologic findings may include increased fibrinogen concentration and nucleated WBC counts. The synergistic hemolysin inhibition test, which detects antibodies to C pseudotuberculosis, can be helpful for detection of internal abscesses.

Treatment consists of poulticing, lancing, flushing, and draining. Occasionally, surgical removal may be required for complete excision. If antimicrobial treatment is used, it should be continued for several weeks.