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 4 of 4

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

 

History
Geographical Distribution
Exposure
How Disease is Triggered
Disease Signs and Effects
Protection
Diagnosis

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 death dealing 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 re-vaccinated 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.