Infectious myopathies involve primary infectious organisms entering muscle tissue in various muscle groups, especially skeletal muscle. These myopathies most often involve bacterial infection and are characterized by inflammation and necrosis. Parasites and viruses are also documented causative agents of infectious myopathies. For example, clinical infection with porcine circovirus 2 in pigs is characterized by multisystemic disease, including development of myositis.
Infectious myopathies are typically characterized by sudden death; fever; muscle swelling and redness (discoloration); crepitation, if gas is present; pain manifesting as lameness; and recumbency. In addition to these clinical signs, elevations in muscle enzymes, as well as bacterial culture from affected muscles, are useful for diagnosis.
Treatment includes supportive care, including analgesia, anti-inflammatory therapy, fluid therapy, fasciotomy to achieve aeration of affected muscle tissue, and targeted therapy with antimicrobials and antiparasiticides where appropriate.
Clostridial Myonecrosis in Ruminants and Pigs
Clostridial infection of skeletal muscle is a noncontagious cause of acute myonecrosis. Infections with Clostridium chauvoei, C septicum, C sordellii, C novyi type B, C perfringens type A, C carnis, or mixed infections involving several agents are common. Clostridia and their spores are ubiquitous in the environment, feces, intestinal tract, and other internal organs of a variety of species. Clostridial myonecrosis can develop after introduction of spores via an IM injection or penetrating wound or through sporulation of organisms already present in muscle when suitable anaerobic conditions are created with muscle trauma.
Any skeletal muscle group in the body can be involved; however, most clostridial infections affect the limb or trunk muscles. Occasionally, muscles such as those around the vulva, tongue, and diaphragm can be involved, or the udder in a cow can be the primary site of sepsis. The release of powerful exotoxins by multiplying clostridia is responsible for local tissue damage, systemic toxemia, and widespread organ dysfunction. The toxins of C sordelli are the most potent of all the clostridial species, and myonecrosis caused by this organism is fatal.
Clostridial infections are characterized by a rapid clinical course, fever (40–41°C [104–106°F]), lameness, systemic toxemia, tremors, ataxia, and dyspnea, often followed in 12–24 hours by recumbency, coma, and death. Mortality can approach 100%. Initially, the skin over the affected area can be swollen, hot, and discolored; however, as the disease progresses, the skin over the area can become cool and insensitive with progressive sloughing. Crepitus might be detectable, indicating subcutaneous gas production.
If a wound is present, a malodorous, serosanguineous discharge might be observed. Hematologic testing and serum biochemical analyses usually reflect hemoconcentration and a stress or toxic leukogram with increased activities of serum CK and serum AST that often do not reflect the toxicity of clostridial myonecrosis.
A definitive diagnosis of clostridial myonecrosis is made from direct smear examination, fluorescent antibody testing, or anaerobic bacterial culture of aspirates of affected tissues. Differential diagnoses include other fulminant disease processes in which there is rapid debilitation or death of the animal.
Clostridial myonecrosis generally has characteristic pathological lesions that are absent in most other conditions, making diagnosis relatively straightforward. Swelling and autolysis are rapid in animals that have died from clostridial myonecrosis, and the carcass usually has a foul odor similar to that of rancid butter. This odor is a characteristic of most cases of clostridial myonecrosis.
C chauvoei infection is characterized by engorgement of the subcutis and adjacent tissues with bloodstained 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 between the separate bundles of muscle toward the center. See the .
Portion of a quadriceps muscle, ex situ, of a 7-month-old heifer, showing a dark, red-purple hemorrhage within the fascia (lower left) and an adjacent cross-section of muscle with a deep, dark red area of hemorrhage (upper right). The heifer was found dead, after an acute history of hindlimb lameness. C chauvoei was identified via fluorescent antibody and culture with mass spectrometry (MALDI-TOF) for identification.
Courtesy of Dr. Michael Rahe and Dr. Rachel Derscheid.
Lesions are similar in sheep and cattle, except that there is usually less gas, and the muscles are not as dry in affected sheep. Myonecrosis resulting from C sordelli 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, affected animals often have massive subendocardial hemorrhages in the left cardiac ventricle and hemorrhage in the trachea, bronchi, and thymus. Extensive perirenal edema and hemorrhagic renal calyces and severe congestion of the lungs are common findings.
Antimicrobial therapy and aggressive surgical debridement might be attempted in the individual animal; however, most cases are fatal. Penicillin G at a dosage of 44,000 U/kg, IM or IV (for aqueous solutions only, such as potassium or sodium penicillin) is the treatment of choice (1). Various frequencies are reported, from every 2–4 hours until the animal is stable (1–5 days) to every 6–8 hours. Use of specific antitoxins is recommended when possible, especially in early stages; however, their effectiveness is questionable. Supportive fluid therapy and use of analgesics and anti-inflammatory agents for control of pain and swelling are recommended. Short-term corticosteroids, including dexamethasone, may be used for initial treatment of systemic and toxic shock; however, continued use is contraindicated in the face of overwhelming sepsis.
Vaccination is recommended beginning at 4–6 months in cattle, with bacterin-toxoids containing antigens against two or more clostridial species, including C chauvoei, C septicum, C novyi, C sordelli, and C perfringens. Two doses of vaccine are necessary to establish good protection. Booster vaccinations should be administered every 6–8 months to maintain protection.
In sheep, naive animals require two doses of vaccination 4–6 weeks apart, followed by yearly boosters. Pregnant ewes may have their booster 3–4 weeks before expected parturition to protect lambs through colostrum. Lambs from unvaccinated ewes should be ≥ 2 weeks old when they receive immunizations (2).
Sarcocystosis in Ruminants and Pigs
Cysts of Sarcocystis are common in the cardiac, esophageal, and skeletal muscle of cattle, sheep, goats, and other species but rarely cause disease. Heavy infestations of Sarcocystis can cause fever, mild anemia, chronic myositis, and muscle wasting.S cruzi, S hirsuta, and S hominis are known to infect cattle, whereas S ovicanis and S capracanis infect sheep and goats. The most common mechanism for natural infection with Sarcocystis in cattle is ingestion of feeds contaminated with infected carnivore feces. (Also see the full discussion of sarcocystosis.)
Key Points
Infectious myopathies of ruminants and pigs are mostly caused by Clostridium.
Acute fatalities and rapid progression of clinical disease are common; therapies might not affect outcomes even when given early.
Vaccinations can decrease the occurrence, severity, and fatal outcomes of clinical disease, particularly in clostridial infections.
For More Information
Constable PD, Hinchcliff KW, Done SH, Grunberg W, eds, Veterinary Medicine: A Textbook of the Diseases of Cattle, Horses, Sheep, Pigs and Goats. 11th ed. Saunders Ltd; 2017.
Smith BP, Van Metre DC, Pusterla N, eds. Large Animal Internal Medicine. 6th ed. Mosby; 2021.
Zimmerman JJ, Karriker LA, Ramirez A, Schwartz KJ, Stevenson GW, Zhang J, eds, Diseases of Swine. 11th ed. Wiley-Blackwell; 2019.
References
Valberg SJ, Spier SJ, Parish SM, Murphy MJ, Carlson GP. Diseases of muscle. In: Smith BP, Van Metre DC, Pusterla N, eds. Large Animal Internal Medicine. 6th ed. Mosby; 2021:1421-1455.e5. doi:10.1016/B978-0-323-55445-9.00042-2
Lacasta D, Ferrer LM, Ramos JJ, Gonzalez JM, Ortin A, Fthenakis GC. Vaccination schedules in small ruminant farms. Vet Microbiol. 2015;181(1-2):34-46. doi:10.1016/j.vetmic.2015.07.018
