Clostridial Myonecrosis

Steven M. Parish • Stephanie J. Valberg

Various species of clostridial organisms cause acute myone­crosis in many farm animal species. Infections are character­ized by a rapid clinical course, fever, systemic toxemia, and high mortality.^85-87 Clostridial diseases are infectious but not contagious.

FIG. 42.7 Clostridial myositis in the left gluteal muscle after an injection of flunixin meglumine, which has progressed to involve the biceps femoris muscle. Fenestrations were created for debridement.

■ Clinical Signs Commonly, clostridial myonecrosis is rapidly progressive with the development of tremors, ataxia, dyspnea, recumbency, coma, and death within 12 to 24 hours. As such, many affected animals may be found prostrate or dead.^85,86,88 Mortality may approach 100%. Affected animals who are still alive are usually severely depressed, febrile (40° to 41° C∕104° to 106° F), tachypneic, anorexic, and lame. These signs are associated with a rapidly developing muscle infection and toxemia. There is usually only one primary site of infection in an affected animal.

Clostridial myonecrosis generally has characteristic patho­logic lesions that are absent in most other conditions, making diagnosis relatively straightforward. Differential diagnoses may include other fulminant disease processes in which there is rapid debilitation or death of the animal.

■ Clinical Pathology Clinicopathologic data alone are seldom specific enough to confirm the presence of clostridial myonecrosis. Hematology and serum biochemical analyses usually reflect a generalized state of debilitation and toxemia (e.g., hemoconcentration and a stress/toxic leukogram may be present). Elevations in the activities of serum CK and serum AST usually occur; however, they often do not reflect the toxicity of clostridial myonecrosis. Aspirates from the affected tissues can yield diagnostic information. It is preferable to obtain tissue specimens for direct smear examination and fluorescent antibody testing, and for anaerobic bacterial culture from affected tissues.

■ Pathophysiology Clostridial agents are ubiquitous in the environment and can frequently be cultured from the feces, intestinal tract, and other internal organs of a variety of species.⁸⁵ Spore-forming characteristics allow these organisms to remain in the environment for long periods, but the exact mechanisms involved in the pathogenesis of clostridial myonecrosis are not fully known.

■ Epidemiology Clostridial agents are common in the environment, and susceptible animals are constantly exposed to them. Areas where previous death losses from clostridial disease have occurred may have a higher incidence or risk of disease because of increased environmental contamination. In cattle, clostridial myonecrosis is generally a disease of animals between 4 and 24 months of age. However, C. sordellii is a more common problem in older feedlot cattle in which excessive muscle bruising may occur.

In sheep and goats, clostridial myonecrosis is most frequently associated with wounds such as those occurring after shearing, docking, and unsanitary surgical procedures. Sheep dipped for parasites after shearing may have an increased risk if the dip becomes contaminated with clostridial spores.

Most reports of clostridial myonecrosis in horses suggest an association with puncture wounds and intramuscular injection sites.^87,89 Intramuscular administration of irritating drugs (includ­ing antihistamines, anthelmintics, and phenylbutazone) may enhance the susceptibility to clostridial myonecrosis. Horses often present with or have a history of another complaint such as colic, exertional myopathy, or laminitis for which they have received injections of drugs in the preceding 48 hours.⁹¹ Previously administered drugs (e.g., phenylbutazone) may mask the fever associated with clostridial myonecrosis, potentially confusing the diagnosis.

■ Necropsy Findings Swelling and autolysis are rapid in animals that have died from clostridial myonecrosis. Blood­stained fluid is often observed discharging from body orifices. Extreme swelling and crepitus may be noted over the affected body area. When acting alone, each of the clostridial agents associated with clostridial myonecrosis produces somewhat different postmortem lesions.

C. chauvoei infection is characterized by engorgement of the subcutis and adjacent tissues with blood-stained fluids and gas bubbles. Cut tissue from the affected area reveals moist, dark-colored muscle in the periphery of the lesion, with lighter colored, drier muscle with gas bubbles separating the separate bundles of muscle toward the center. Other changes include severe degeneration of parenchymatous tissues caused by the systemic toxemia. The carcass usually has a foul odor similar to that of rancid butter. This odor is a characteristic of most cases of clostridial myonecrosis. The lungs are often congested with edema, and hemorrhage and a fibrinohemorrhagic pleuritis are common. The heart may be friable and show evidence of endocardial hemorrhages, particularly on the right side. The spleen may be normal or enlarged and friable. The liver is usually pale and friable and may be autolytic and porous. Lesions are similar in sheep and cattle, except that there is usually less gas and the muscles are not as dry in affected sheep.

Similar necropsy findings are found with myonecrosis caused by C. septicum and C. novyi type B. C. septicum and C. perfringens generally occur as part of mixed wound infections in which abundant malodorous, serosanguineous fluid is found at the wound site. C. perfringens is common in horses.

Myonecrosis resulting from C. sordellii is most often associ­ated with lesions of the neck or brisket area of cattle. Death is frequently so rapid that subcutaneous gas accumulation is rare. In addition to local myonecrosis, these animals often have massive subendocardial hemorrhages in the left ventricle of the heart and hemorrhage in the trachea, bronchi, and thymus. Extensive perirenal edema and hemorrhagic renal calyces and severe congestion of the lungs are common findings.

■ Treatment Although clostridial myonecrosis is often fatal, aggressive specific therapy combined with supportive care may be successful in individual cases.

Surgical intervention at the affected site by means of debride­ment or fenestration in an attempt to reduce tissue swelling, aerate the tissues, and remove necrotic tissue is considered imperative for survival in horses (see Fig. 42.7). Incisions are made through the skin and into the affected muscle to establish adequate drainage and hopefully alter the anaerobic conditions. Sufficient fenestrations should be made to establish drainage and aeration over the entire affected area.

Use of specific antitoxins is recommended when possible. However, these are often not available or not used for immediate therapy because the exact species of Clostridium causing the myonecrosis is not known. Cost considerations may also preclude their use. Supportive fluid therapy and use of analgesics and anti-inflammatory agents for control of pain and swelling are rec­ommended. Short-acting corticosteroids such as dexamethasone, prednisolone, or hydrocortisone may be used for initial therapy of systemic and toxic shock, but continued use is contraindicated in the face of overwhelming sepsis. If required, specific therapy should also be directed toward any other underlying problems.

■ Prognosis The prognosis for life in all cases of clostridial myonecrosis is guarded to poor. The disease process is often rapidly fulminant, making treatment unrewarding. However, some animals have survived because of early diagnosis, aggressive therapy, and long-term supportive care. This is particularly true in cases involving C. perfringens in horses. The owner should be aware from the start of treatment that extensive skin sloughing may involve most of a limb and may force euthanasia to become a consideration at a later stage.

■ Prevention Protection against clostridial myonecrosis is based on immunization procedures. Although clostridial agents are ubiquitous in the environment and frequently appear in the body of susceptible animals, rarely does adequate natural protec­tion occur, although some colostral and acquired immunity may at times occur. Infection in unprotected animals usually follows a rapid, degenerative clinical course and terminates before the animal can generate an appropriate protective immune response. At present, only ruminants are commonly vaccinated against the agents responsible for clostridial myonecrosis. Vaccines used include multivalent bacterin toxoids containing antigens against two or more clostridial species, including C. chauvoei, C. septicum, C. novyi, C. sordellii, and C. perfringens. A rational program for protection usually involves vaccinating at an early age to establish immunity. Vaccination age is partly determined by other management factors, including when calves are handled for branding and castration, but 4 to 6 months of age is the usual time of initial vaccination. In areas of heavy exposure it may be necessary to vaccinate at 3 months and again at 4 months. In all clostridial species except C. chauvoei, two doses of vaccine are necessary to establish good protection. The duration of immunity is not long, and booster vaccinations should be administered every 6 to 8 months if protection is to be maintained. In many herds it is only necessary to vaccinate animals younger than 3 years of age (i.e., those animals that are at greatest risk), but in some high-risk herds it is necessary to maintain a vaccination program for the life of the animal.

Animals that die of clostridial diseases should be disposed of by deep burial, burning, or removal from the premises to avoid further contamination of the environment.