THE MERCK VETERINARY MANUAL
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Infectious Myopathies in Horses

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Virus-Associated Myositis

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.

Sarcocystis Myositis

Cysts of the sporozoan parasite Sarcocystis are present in 90% of esophageal muscles from horses >8 yr of age and in 6% of gluteal muscle biopsies from healthy horses. Occasionally, heavy infestations occur through contamination of feed with canine feces, resulting in 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.)

Anaplasma-Associated Rhabdomyolysis

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. A diagnosis is confirmed by PCR testing of blood for A phagocytophilum. A direct toxic effect of A phagocytophilum on muscle cells is postulated. Treatment should include IV oxytetracycline and supportive care.

Streptococcus equi Rhabdomyolysis

Severe rhabdomyolysis can occur in horses with Streptococcus equi equi submandibular lymphadenopathy and/or guttural pouch empyema. A stiff gait is the initial clinical sign, which progresses rapidly to severely painful, firm, swollen epaxial and gluteal muscles. Many horses become recumbent with unrelenting pain that may warrant euthanasia. It is not clear whether myonecrosis is a direct toxic effect of S equi on muscle cells or is due to profound nonspecific T-cell stimulation by streptococcal superantigens and the release of high levels of inflammatory cytokines. A diagnosis is based on hematologic abnormalities typical of S equi infection, marked increases in CK (>100,000 U/L), and PCR or bacterial culture. Titers to the M protein of S equi are low in affected horses, unless they have recently been vaccinated for strangles. At postmortem, large, pale areas of necrotic muscle are evident in hindlimb and lumbar muscles. The histopathologic lesions are characterized by severe acute myonecrosis with a degree of macrophage infiltration. Sublumbar muscles often show the most severe and chronic necrosis, as indicated by greater macrophage infiltration of myofibers. The prognosis becomes guarded if animals become recumbent.

Appropriate therapy includes IV penicillin combined with an antimicrobial that inhibits protein synthesis, such as rifampin. Flushing infected guttural pouches and draining abscessed lymph nodes will diminish the bacterial load. NSAIDs and possibly high doses of short-acting corticosteroids may diminish the inflammatory response. Control of unrelenting pain is a major challenge in horses with severe rhabdomyolysis. Constant-rate infusion of lidocaine, detomidine, or ketamine may provide better anxiety and pain relief than periodic injections of tranquilizers. Horses should be placed in a deeply bedded stall and moved from side to side every 4 hr if they are unable to rise. Some horses may benefit from a sling if they will bear weight on their hindlimbs when assisted to stand.

Clostridial Myositis

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, whereas 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 powerful exotoxins. Within 48 hr, horses show depression, 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 hr. Myocardial damage occurs in some horses. Hematology and serum biochemical analyses usually reflect a generalized state of debilitation and toxemia (eg, hemoconcentration and a stress/toxic leukogram may be present). Serum CK and AST are usually moderately increased; however, they often do not reflect the toxicity 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, swelling, crepitus, and autolysis are rapid, and bloodstained fluid is often seen 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 IV potassium penicillin every 2–4 hr until the horse is stable (1 to 5 days), combined with or followed by oral metronidazole along with supportive fluid therapy and anti-inflammatory agents. Extensive skin sloughing over the affected area is common in surviving horses.

Muscle Abscesses

Staphylococcus aureus, Streptococcus equi, and Corynebacterium pseudotuberculosis are common causes of skeletal muscle abscessation, which develops 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. Ultrasonography and culture of aspirated fluid are the best means of diagnosis in superficial sites. Abscesses lying deep within muscles can be difficult to diagnose. There may be an increased fibrinogen and nucleated WBCs. 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 therapy is used, it should be continued for several weeks.

Last full review/revision February 2014 by Stephanie J. Valberg, DVM, PhD, DACVIM, ACVSMR

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