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)
Organism
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Disease
Name
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Muscle
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Liver
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Gut
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Cl. chauvoei
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Blackleg
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Cl. septicum
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Malignant Edema
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+
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Cl. sordellii
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"Sord"
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+
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Cl. tetani
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tetanus
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+
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History
Geographical Location
How Exposure Occurs
How Disease is Triggered
Disease Signs & Effects
Protection
Diagnosis
Return to Q & A
Page
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 revaccinate at weaning
or four to six months of age.
In breeding herds, all animals should be revaccinate 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.
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