10 Infectious myositis
10.1 Clostridial myositis
Clostridial infections are common and important diseases of livestock. Common causes of clostridial disease are C. septicum, C. chauvoei, C. perfringens, C. novyi, and C. sordellii. Occasionally more than one species can be cultured. Although the following conditions are often attributed to specific clostridial species, these should be considered the most common cause, and not necessarily the sole cause. Clostridial disease is caused by the release of exotoxins, leading to local damage and systemic illness. They are often fatal.
A common thread in the pathogenesis of clostridial myositis is the prerequisite for muscle with reduced oxygen tension that leads to vegetative growth of the organism and the production of damaging exotoxins. Further detail is found in the sections below.
10.1.1 Malignant edema and gas gangrene
Malignant edema and gas gangrene are two forms of clostridial myositis, occurring most commonly in the horse but also in cattle and other livestock. They share a pathogenesis and many clinical signs; it is simply the presence of gas bubbles that distinguishes gas gangrene from malignant edema. C. septicum is most commonly the cause of malignant edema, while C. perfringens is more frequently isoltaed from gas gangrene.
Malignant edema/gas gangrene occurs following the introduction of spores by a deep, penetrating wound, almost always from an injection, though surgical procedures (castration) may also contribute. Local anaerobic conditions allow organisms to proliferate and produce exotoxin that damage blood vessels and myofibers, causing hemorrhage and myonecrosis. The damage is often extensive and accompanied by a serosanguineous exudate and extremely foul smell. Microscopically, hemorrhage, edema, and myonecrosis predominate. Neutrophils and bacteria are present but are infrequent. Without prompt treatment (antibiotics and fasciotomy, Figure 10.1), death occurrs within 24-48 hours.
Figure 10.1: Malignant edema in a cow resulting in marked swelling of the gluteal muscles. This cow was treated with several fasciotomy incisions to release the pressure and allow exposure to oxygen. Image courtesy of Dr. H Staempfli, OVC.
10.1.2 Blackleg
Blackleg is a common and deadly condition of well-conditioned, pastured cattle 9 months to 2 years old. The cause of blackleg is C. chauveoi. Unlike malignant edema/gas gangrene, penetrating wounds are not a feature of blackleg. Instead, spores are ingested from contaminated pasture, and, through as yet unknown mechanisms, cross the intestinal mucosa and spread hematogenously to various organs, including skeletal muscle. It is only when an event creates muscle damage or leads to low muscle tension that the disease manifests. Low oxygen tension creates the right environment for spores to germinate and for organisms to multiply and release toxin, leading to vascular necrosis, hemorrhage, and myonecrosis. Lesions are most frequently found in the muscles of the limbs, though the tongue and diaphragm are also common sites. The myocardium may also be affected. The clinical course is so rapid that clinical signs are rarely observed; animals die within 24-36 hours.
The condition derives its name from the gross appearance of muscle at necropsy, which is typically dark red to black, with or without gas bubbles. Histologically, severe myonecrosis and fragmentation are present alongside marked edema and hemorrhage.
10.1.3 Botulism
Note: Botulism and Tetanus are described here, as they are clostridial diseases, but they should be considered neuromuscular diseases. They do NOT cause a myositis!
C. botulinum is the causative agent of botulism, a neuromuscular disease leading to flaccid paralysis of skeletal muscle. Horses are particularly susceptibe. In foals < 6 months of age, ingestion of C. botulinum spores can lead to proliferation of the organism and production of botulinum toxin. In adult horses, it is more commonly the ingestion of botulinum toxin, not the bacteria itself, that is the cause of the disease. Hay contaminated with the corpses of rodents is a common source of botulinum toxin. Botulinum toxin spreads hematogenously to the neuromuscular junction where it is taken up by the terminal axon. Botulinum toxin binds to synpatic vesicles containing acetylcholine, preventing their release, and thereby preventing the spread of action potentials, ultimately resulting in paralysis. There are no gross or histological lesions.
10.1.4 Tetanus
Like Botulism, tetanus is the result of a clostridial toxin affecting neurotransmitter release. It develops when spores of C. tetani are introduced into tissue by penetrating injuries. Anaerobic conditions at the site of injury prompt the spores to vegetate. Tetanus toxin is taken up by endocytosis into the axon of the nearest motor neuron and brought via retrograde transport to the neuronal cell body within the spinal cord. There the tetanus toxis is released, and is then taken up by the axon of an inhibitory neuron. Once within the inhibitory neuron, the toxin acts in a fashion similar to that of botulinum toxin, and interferes with the release of acetylcholine. It is the abolishment of inhibitory signals that leads to the clinical signs associated with tetanus. Motor neurons are under more or less constant stimulation, and the inhibitory neurons serve to counter balance this stimulation. With the removal of inhibitory constraint, all that is left is stimulation, leading to prolonged, severe muscle contraction.
Horses, guinae pigs, and humans are most susceptible to disease, while dogs and cats are relatively resistant. There are no gross or histologic lesions.
10.2 Suppurative myositis
Suppurative myositis is most commonly the result of innoculation from trauma or surgery. Occasionally, abscesses can develop in muscle through extension from nearby structures (e.g. joint or tendons), or through hematogenous spread. The most common bacterial isolates from muscle abscesses are given in Table 10.1.
| Species | Bacteria |
|---|---|
| Cattle | T. pyogenes |
| Swine | C. pseudotuberculosis, H. parasuis |
| Sheep | C. pseudotuberculosis |
| Goats | C. pseudotuberculosis |
| Horses | C. pseudotuberculosis, S. equi |
| Cats | P. multocida |