Clostridial myositis is an infection of muscle by Clostridium spp. most frequently associated with IM injection. The infection may remain localized and form a focal abscess or migrate along fascial planes, resulting in diffuse necrotizing cellulitis.
The frequent temporal association between IM injections and clostridial myositis suggests entry of the organism at the time of injection. However, injection of irritating substances may produce local tissue necrosis and an anaerobic environment ideal for proliferation of spores that may already be present in muscle. Because of the ubiquitous nature of clostridial organisms both in the environment and as commensals in the horse, they may contaminate wounds and surgical sites. The release of potent clostridial exotoxins leads to local tissue necrosis, systemic toxemia, and organ dysfunction. In this most severe form, the term malignant edema is used to reflect the systemic involvement and high mortality.
This is the primary system affected. Necrotizing toxins released by the organism lead to local soft tissue necrosis. Osteitis of cervical vertebrae in close proximity to the infection may occur.
Exotoxins absorbed from the site of infection may induce intra- or extravascular hemolysis and increased capillary permeability. Transient hypertrophic cardiomyopathy has been documented.
Some geographic areas may have a greater incidence owing to higher environmental contamination by clostridial organisms.
IM injection with a non-antibiotic medication is the most common cause of clostridial myositis, and thus owners should be questioned about recent medications, treatments, or illnesses. Depending on the site of infection, horses may be stiff and reluctant to walk, lame, or unwilling to raise or lower the head to eat. Pain and systemic toxemia may lead to anorexia and tachypnea. Vague signs of discomfort are easily mistaken for colic.
If myonecrosis is related to IM injection, common sites of injection should be palpated for heat, pain, swelling, and crepitus. Small puncture wounds are occasionally only visible once the hair over the affected area is clipped. Swellings are initially warm and painful and later become cool, firm, and necrotic. Muscle pain may cause a lame or stiff gait, reluctance to walk, depression, anorexia, tachypnea, and tachycardia. Dehydration, depression, delayed CRT, poor peripheral pulses, and cool extremities suggest systemic toxemia and inadequate peripheral perfusion and shock. Oral mucous membranes may be dark red to blue. Fever is common.
Clostridial myositis is most often associated with Clostridium perfringens (type A) and Clostridium septicum, but Clostridium chauvoei, Clostridium novyi, Clostridium fallax, and Clostridium sordellii have also been reported.
Although any IM injection could potentially result in a clostridial infection, medications that are irritating and result in tissue necrosis are frequently associated with this syndrome. Flunixin meglumine is most commonly implicated; however, IM injection of other medications such as xylazine, ivermectin, vitamin B complex, antihistamines, phenylbutazone, dipyrone (metamizole), synthetic prostaglandins, and vaccines have also been associated with clostridial myositis.
When clostridial myositis is secondary to an injection, the diagnosis can be complicated by previous medical problems. Pain associated with myonecrosis may be confused with colic, exertional myopathy, laminitis, or abscesses from other causes. Severe pain, fever, toxemia, and shock rarely result from an abscess due to other less virulent organisms.
If clostridial infection is localized into an abscess, a CBC may reveal only a modest leukocytosis with left shift and neutrophilia. Hyperfibrinogenemia may be present if infection is present for more than a few days. When severe systemic toxemia develops, anemia, leukopenia, thrombocytopenia, and intra-/extravascular hemolysis can occur. If IMHA is present, spontaneous autoagglutination may be seen. Increases in muscle enzymes creatine kinase and aspartate aminotransferase may be mild compared with the apparent severity of toxemia perhaps due to the focal nature of the disease, destruction of enzyme, or lack of enzyme absorption into the systemic circulation. Dehydration and shock may result in azotemia and hemoconcentration. Increases in hepatic enzymes, total bilirubin, and bile acids may occur. Hemoglobinuria/myoglobinuria may be present. Urinalysis results should be evaluated with the serum chemistry to measure renal insult.
Clostridial toxins may result in DIC and alterations in clotting factors. Elevation in cardiac troponin I may suggest myocardial injury and should be paired with echocardiography. A direct Coombs test may be positive in cases developing IMHA.
Ultrasonography may reveal an encapsulated abscess or diffuse tissue edema, necrosis, cellulitis, and echogenic foci of emphysema. Differentiation between focal abscesses and diffuse cellulitis aids in defining areas for treatment. Abscesses should be lanced and lavaged. Fasciotomy/myotomy is appropriate if diffuse cellulitis and myonecrosis are present.
A tentative diagnosis can be made based on a history of IM injection or wound and a rapid onset of clinical signs. Diagnosis can be confirmed by aspiration of purulent or serosanguineous material for anaerobic culture, cytology, or fluorescent antibody identification. Care should be taken to properly prepare sites for aspiration to avoid contamination with surface organisms. Samples should be collected and placed in a medium designed for transportation of anaerobic specimens and submitted to a laboratory as soon as possible. Muscle biopsies frequently reveal characteristic Gram-positive rods.
Treatment options are dictated by the severity of the disease. Focal encapsulated abscesses may be managed in the field; however, referral should be considered for horses with signs of systemic toxemia (tachycardia, increased CRT, abnormal mucous membrane color, poor peripheral pulses, or cool extremities).
Oral or parenteral fluids are indicated if dehydration is present and balanced polyionic fluids (lactated or acetated Ringer's solution) should be administered IV if there are signs of shock. Hot-packing may aid in drainage of abscesses, whereas later in the course of the disease cold hydrotherapy may decrease the activity of inflammatory mediators. Feed and water should be provided at head level for horses with neck pain associated with infection of cervical musculature.
Clients should be educated on which medications are appropriately given IM. Alternate routes of administration for certain medications, such as orally for flunixin meglumine, should be emphasized.
Focal abscesses may be drained by incision, lavage, and placement of a drain. Diffuse cellulitis and tissue edema are important to identify echographically because medical management may be more appropriate for this type of infection. Depending on the severity of the disease, fenestration of infected tissue with vertical incisions is helpful in reducing an anaerobic environment. Incisions are made through skin and necrotic muscle so as to aerate tissues and reduce pressure associated with severe edema. Minimal sedation and hemostasis are frequently necessary owing to the necrotic nature of the tissue incised.
Hydration and renal function should be monitored when using nonsteroidal anti-inflammatory medications in horses with severe systemic disease.
Avoiding IM injection of irritating or frequently implicated medications may reduce the incidence of Clostridium myositis.
Severe toxemia may lead to shock, renal insufficiency, hepatobiliary insult, laminitis, intravascular hemolysis, cardiomyopathy, DIC, collapse, or death.
Small, focal abscesses may respond well to drainage and systemic antimicrobials. Horses with diffuse myositis, toxemia, and shock have a guarded to poor prognosis in spite of aggressive therapy. C. septicum and C. chauvoei infections are usually fatal; however, C. perfringens infections have a better prognosis.
Peek SF, , . Clostridial myonecrosis in horses (37 cases 19852000). Equine Vet J 2003;35(1):8692.
Rebhun WC, , , et al. Malignant edema in horses. J Am Vet Med Assoc 1985;187:732736.
Author: Liz Arbittier
Consulting Editor: Ashley G. Boyle
Acknowledgment: The author and editor acknowledge the prior contribution of Kerry E. Beckman.
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