Gastrointestinal Group
Clostridial Disease (Enterotoxemia) which effects the Gastrointestinal
Group of cattle, sheep, goats, swine and horeses include cl. perfringens,
types B, C, and D.
Information supplied from Schering-Plough
Animal Health Corp. information booklet, Clostridials, (SPAH-BOV-94)
Page 4of 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. perfringens, Type B |
Enterotoxemia |
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| Cl. perfringens, Type C |
Enterotoxemia |
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| Cl. perfringens, Type D |
Enterotoxemia |
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History
Geographical Distribution
Exposure
How Disease is Triggered
Disease Signs and Effects
Protection
Diagnosis
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History
Cl. perfringens has long been clearly recognized as a disease
of livestock which is of distinct economic significance.
The organism was first isolated from a human cadaver in 1892. Probably
because of its pathogenicity in humans as well as livestock, it has been
the subject of considerable research throughout the years. As a result,
the body of information relating to it is more extensive than that of
any other clostridial species with the possible exception of Cl. tetani.
In livestock, Type c received early recognition for its effects in sheep,
particularly young nursing lambs and older lambs placed on lush pasture
or rich feed. Type C was similarly recognized as the cause of losses in
young calves and pigs, causing a fatal form of enteritis.
In recent years, changes in cattle husbandry, particularly the use of
high energy feeds in feedlot cattle and dairy cows, have led to and increasing
number of reports of Type D infections in this animal species. There is
evidence that Type D may currently be of greater significance in cattle
than type C.
Geographical Distribution
Cl. perfringens is considered to be worldwide in its distribution.
Almost every sample of soil that has ever been examined, with the exception
of the sands of the Sahara, has been found to contain certain types of
this species.
Cl. perfringens has been found, in varying numbers, in the intestinal
contents of all of the many animal species that have been investigated.
The number of organisms per gram of feces is significant, but varies from
species to species and individual to individual.
Although cases have been confirmed, Type B has not been generally regarded
as a significant problem in the U.S.A. whether this is an accurate picture
of the incidence of this type or only a mistaken impression caused by
the difficulty in obtaining a definitive diagnosis is not clear.
Exposure
The potential for exposure to disease-causing bacteria of the gastrointestinal
group can be considered constant. These bacteria revert from the spore
form to the nonspore form upon locating in the small intestine. Conditions
which reduce oxygen availability can stimulate multiplication of bacteria
and their release of destructive toxins.
How Disease Is Triggered
The diseases of the gastrointestinal group appear following the intake
of feeds high in soluble carbohydrates and/or when the diet is changed
suddenly. Although the events leading to accelerated multiplication of
resident bacteria have not been fully established, the circumstances are
felt to be as follows: Excess ingestion of feed brings about a change
in the rumen flora from a predominantly gram negative bacterial population
to one that is gram positive. The latter ferment grain to lactic acid,
producing acidosis. Partially fermented grain is allowed to enter the
small intestines mainly in the form of starch granules. This creates an
environment favoring rapid multiplication of Cl. Perfringens Type
D. As acidosis worsens, the motility of the rumen and intestinal tract
decrease. This allows epsilon toxin produced by the growing bacteria to
accumulate in the forward part of the small intestine. This toxin facilitates
its own escape into the bloodstream by increasing the permeability of
the intestinal mucosa.
Cl. Perfringens Type C is activated under conditions in the small
intestine produced by large quantities of milk, intestinal stasis and,
possibly, a lack of exercise. Upon activation, bacteria multiply and release
a beta toxin with potent necrotizing and lethal properties.
Disease Signs and Effects
Deaths from diseases of the gut group occur suddenly, usually before
clinical signs are seen. When observed, the signs in cattle and sheep
are similar. Cl. perfringens Type D generally produces a pure toxemia.
Lethal toxins are produced by rapidly growing bacteria which readily penetrate
the intestinal wall and are distributed by the bloodstream to other systems
and organs where deathdealing effects are produced.
In Type D disease, special signs include nervousness (excitement), convulsions,
coma and death. They are similar to those seen in polioencephalomalacia
and thromboembolic meningoencephalitis (TEME). This is caused by the neurotrophic
effects (nerve tissue effects) of the epsilon toxin released by this organism
type.
In Type C disease, signs include abdominal pain (colic), depression and
"low bloat." In lingering cases, blood is observed in the feces
and surviving animals are usually unthrifty. The signs of Type C result
from the action of a necrotizing (tissue destroying) beta toxin that produces
sever inflammation and hemorrhage of the intestinal lining, often referred
to as "purple gut."
Protection
Routine vaccination is the only practical way to insure against losses.
Such vaccination will not prevent Cl. perfringens organisms from
multiplying and producing toxins. It will, however, stimulate the animal
to produce an advance protective response (antitoxin) capable of neutralizing
lethal toxins.
In designing the vaccination program, careful consideration should be
given to the class of animals requiring protection. The guiding rule should
be to time vaccination before periods of extreme risk. Such periods include
finishing in feedlots, grazing on lush pastures, growing on creep feed
or milk replacers, and the intake of rich mother’s milk.
Animals vaccinated for the first time should receive two doses spaced
three to four weeks apart. If vaccinated before three months of age, vaccination
should be repeated at weaning or five to six months of age. In breeding
herds, all animals should be revaccinated annually.
Protection of young nursing animals is best achieved through vaccination
of the dam. This provides protective antibodies in the first (colostrum).
Diagnosis
Diagnosis can be attempted on a presumptive basis at the time a dead
animal is posted. The presence of generalized inflammation or extensive
hemorrhagic lesions may indicate Type C or Type B as the primary offender.
Type D is more apt to be a pure toxemia without gross lesions.
Positive diagnosis is generally dependent on laboratory identification
of and offending toxin. The diagnostician must deal with a potential of
12 known toxins. Three of these, Alpha, Beta and Epsilon, are regarded
as major lethal types.
Toxins are obtained from intestinal contents and analyzed through tests
in mice. It is well to remember that these toxins are easily destroyed
by postmortem autolysis and may not be detectable in specimens received
by diagnostic laboratories.
The fluorescent antibody test is considered a useful diagnostic tool
to evaluate the concentration of these bacteria in the intestinal tract.
Concentrations considered unusually high can indicate that an activating
condition and consequent bacterial multiplication has occurred.
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