Muscle Group

This section will discuss the Clostridial diseases of the muscle group of cattle, swine, goats, sheep, and horses regarding cl. chauvoei (blackleg), cl. septicum (Malignant Edema), cl. sordellii (Sord), cl. tetani (tetanus).

Information supplied from Schering-Plough Animal Health Corp. information booklet, Clostridials, (SPAH-BOV-94)

Page 2 of 4

Closdridial Diseases of Livestock (Page 1)
Muscle Group. (Page 2)
Liver Group. (Page 3)
Gastrointestinal Group. (Page 4)

 

History
Geographical Location
How Exposure Occurs
How Disease is Triggered
Disease Signs & Effects
Protection
Diagnosis

History

It is not known how long the clostridial diseases whose principal infection site is the muscle have been recognized. The literature refers to severe outbreaks of blackleg (Cl. chauvoei) almost a century ago.

The seriousness of these diseases is clearly illustrated by the fact that early research workers attempted to control blackleg losses with a crude vaccine prepared from dried fluids of disease lesions even before the causative organism was identified.

As time passed, specific organisms that produced gangrenous muscle diseases were identified. The first was Cl. chauvoei, the cause of blackleg. Then came Cl. septicum, the cause of malignant edema, and Cl. sordellii, the cause of a disease variously known as "Sord," blackneck, etc.

Vaccine development followed close on the heels of organism identification. Livestock losses were reduced by the first vaccine which contained only Cl. chauvoei. Losses were further reduced through use of a vaccine containing Cl. septicum. A single vaccine containing both Cl. chauvoei and Cl. septicum was soon developed, the use of which has continued to the present. In recent years, Cl. sordellii and Cl. tetani have has been incorporated into vaccines, making it possible to vaccinate against all significant clostridial disease whose principal infection site is the muscle.

Geographical Distribution

Clostridial diseases of the muscle group are widespread. The causative bacteria are natural habitants of soil, and readily take up residence in the bodies of animals. This follows either the intake of contaminated feed and water or entry via wounds and scratches. They may be distributed to tissues throughout the body where they remain latent (nonactive) until an activating condition occurs.
The spread of these diseases from premise to premise and area to area is aided by the excretion of causative organisms by healthy carrier animals or from the carcasses of animals that were diseased. All factors considered, the potential for these diseases is a constant threat wherever livestock are raised and/or fed.

How exposure Occurs

Spores residing within the animal body must be considered a potential source of infection. They become a source of infection upon being activated by conditions which destroy tissue, reducing the local supply of oxygen.

How Disease Is Triggered

Conditions, irrespective of cause, that impede the circulation of oxygen-carrying blood, create an anaerobic environment that can result in the germination of local spores (one or all three clostridial species). Such conditions can result from the activity of animals in nature and under conditions of managed husbandry. Conditions in nature, which cause muscle damage, include bruises caused by butting, riding (i.e., estrus in cows and buller steers), scratches and wounds. Those under confined husbandry conditions include bruises from close confinement, banding bulls, feed bunks, shipping and restraint in squeeze chutes, alley, etc. Seldom does a stockman view the methods used to "prod" animals as a trigger for clostridial diseases of the muscle.

Disease Signs and Effects

These diseases are characterized by swelling, edema and sometimes emphysema (gas) in the muscle tissues surrounding the area of infection. These swellings are seen most often in the area of the hip, shoulder, neck and upper leg. Affected animals are usually lame and depressed. Their body temperatures are elevated during the early phase of disease-below normal as the disease progresses. In the final stages, depression worsens and the animal goes down. Death usually occurs within 12 hours after the appearance of clinical illness.

Events underlying visible clinical signs include: Toxins release by growing bacterial produce widespread muscle damage (gangrenous myositis). These toxins are absorbed by the bloodstream (toxemia) and are dispersed throughout the body where they cause damage and impair the function of life-sustaining organs and systems.

Cl. chauvoei produces less toxin but more tissue damage and emphysema (gas) than do Cl. septicum and Cl. sordellii. The latter species produce high amounts of toxins. The toxin of Cl. sordellii is considered by many to be the most potent of this muscle group.

Protection

Acute clostridial infections usually produce death before the body can mount a life-saving defensive response. For this reason, it is essential that animals be immunized before conditions responsible for bacterial growth occur.

Animals being vaccinated against diseases of the muscle group for the first time should receive two doses three to four weeks apart. Animals vaccinated under three months of age should be re-vaccinate at weaning or four to six months of age.

In breeding herds, all animals should be re-vaccinate annually. This maximizes the protection of brood cows and also helps assure that their calves will receive high levels of protection from first milk.

Diagnosis

Clostridial diseases of the muscle group are a consideration in any cases of sudden death in susceptible animal species. If clinical illness is noted before death, a presumptive diagnosis of Cl. chauvoei and/or Cl. septicum is possible, based in such signs as swelling, crepitation, lameness, etc. Cl. sordellii usually produces death before visible signs are apparent.

Postmortem findings: The principal lesion of Cl. chauvoei in cattle is found in voluntary muscle. Most often, it is seen in the large muscle masses of the hip, shoulder, thigh or neck. On rare occasions it may be located in the tongue, the jaw muscles, or even the diaphragm. The affected muscle is dark reddish-brown in color, with the cut surface being "dry." In sheep, the principal finding is a gangrenous infection of external wounds.

The lesions produced by Cl. sordellii and Cl. septicum are similar to, but not as extensive as those of Cl. chauvoei. More extensive edema is present as a result of the greater amounts of toxin produced by these two agents.

Laboratory Analysis: Fresh specimens of affected muscle and surrounding tissue provide the laboratory diagnostician with the best opportunity to identify the causative agent(s). Autolysis occurring in aged field collected specimens can render differential diagnosis difficult, if not impossible.