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Clostridial diseases (black, bacillary, hemoglobinuria, redwater) which effect the liver. cl. novyi, also known as cl. haemolyticum. Affecting cattle, sheep, goats, swine and horses.
Information supplied from Schering-Plough Animal Health Corp. information booklet, Clostridials, (SPAH-BOV-94)
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The identity of the two clostridial organisms whose principal infection site is the liver dates back to the late 1800s and early 1900sd. Since that time, they have been variously regarded as either two types of the same clostridial species (Cl. novyi Type B and Type D), or as two distinct species (Cl. novyi and CL haemolyticum). The latter view is based primarily on differences and disease manifestations.
The pathogenic (disease producing) characteristics of these two clostridial organisms are quite similar, for liver tissue and both are dependent on some form of liver damage for the activation of latent spores.
This has been confirmed through a series of studies in cattle. When live spores of Cl. novyi type or type D were inoculated, along with a tissue debilitant to the liver, 85 to 100% of the rest animals died. When this same material was inoculated into muscle, deaths from Type D did not occur at all, and death from Type B did not occur consistently. These results indicate that although Type B infections in the muscle are possible, such tissue is not the optimal site for multiplication of these organisms.
Laboratory and field evidence shows the disease of the liver group to be widespread.
Early, it was the belief that both type B and type D infections were threats only in a limited number of areas, and that the diseases occurred only in poorly drained pastures suspected of being "hot spots" for soil-borne spores. It is now believed that higher incidence of disease in these areas is more a function of liver damage created by parasitic flukes which abound in such areas than the presence or absence of soil-borne spores.
The improvement of transportation systems (the trucking industry, primarily) and the expansion of livestock raising and feeding into new areas have greatly increased the movement of animals from region to region. Realizing that clostridial spores are spread through excretions, etc., there is probably no region in the United States where these diseases are not a threat.
The risk to feedlot and dairy animals has been increased as the result of liver stress produced by the use of high performance rations. Cl. novyi diseases in feedlot animals is not a recent finding. Heavy losses were described over fifty years ago by Records and Vawter among cattle eating hay cut from infected fields (University of Nevada Technical Bulletin, 1945). These pioneering workers also stated, "Cases have occurred in feeder cattle originating in regions where the disease was prevalent, the ranch or feed yards at destination having shown no former evidence of it." The authors of Diseases of Cattle (Second edition, American Veterinary Publications, Inc.) stated "… the disease has occurred as long as one month after arrival at a farm or feed yard at which there has been no previous evidence of it."
As with the muscle group, spores which reside within the animal are always a potential source of infection. Infection occurs when activation conditions make it impossible for the bacteria to multiply and release destructive toxins.
Spores of the liver group enter the body through contaminated feed ant water. They do not usually enter through wounds and scratches as do Cl. septicum and Cl. sordellii. A reservoir is established in the intestinal tract from which spores enter the bloodstream for distribution to the liver and other tissues of the body.
Some form of liver damage is required for activation of the spores. As with organisms of the muscle group, triggering conditions are those that impede blood circulation, damage or destroy cells, and reduce oxygen availability.
Common sources of liver damage include abscesses, chemicals, fatty changes, internal parasites, flukes, plant toxins, sawdust liver (telangiectasis) and bacterial or viral hepatitis.
In he presence of liver damage, latent spores germinate. Potent toxins are produced which expand the area of tissue damage. Toxins are also absorbed by the bloodstream through which they reach and damage life-sustaining organs and systems. A unique effect is the interruption of the oxygen-carrying capacity of the blood through destruction of red blood cells and the linings of small blood vessels.
These diseases follow a rapid course. The acute stage is usually reached before outward signs appear. Often animals are found dead before clinical signs are observed.
If observed, early signs include depression and fever. Animals stand apart from the herd and are reluctant to move. Many will assume an arched back posture with neck extended. As the disease progresses, breathing becomes difficult and blood-tinged froth may appear in the nostrils. In lingering cases of Type D, the passage of red-color urine (hemoglobinuria) may occur, but may not be observed.
The nature of the diseased in the Cl. novyi group makes routine vaccination essential. As with all clostridial diseases, affected animals rarely get a second chance; death usually occurs faster than the body can mount a defensive response. Those being vaccinated for the first time (primary immunization) should receive two doses three to four weeks apart. Those vaccinated under three months of age should be revaccinated at weaning or five to six months of age. Subsequent to this, animals should be revaccinated every five to six months.
The degree of liver stress resulting from any management program should be considered. Stock should be revaccinated prior to periods of special risk of such as pastures infested with snails (the liver fluke intermediate host) and being placed on a concentrated feeding program.
As with the clostridial diseases of the muscle group, diagnosis of clinical disease caused by Cl. novyi Types B or D may not be possible due to the brevity of clinical illness prior to death. If clinical signs of infection with Type D persist beyond 24 hours, and if affected animals are observed frequently enough, a presumptive diagnosis may be made on the basis of hemoglobinuria which may be observed. In most cases, however, animals will be found dead.
Postmortem diagnosis of death due to acute cases of CI. Novyi Types B or D presents a challenge in differentiating between the tow because of similarities in gross pathology. Lesions of acute toxemia are present, accompanied by varying degrees of edema and hemoglobin-containing fluid in body cavities. Carcasses of animals which have died as the result of Type D infections may exhibit more extensive evidence of hemolysis and may have red urine in the bladder. These signs, however, may not be found at all in animals that have died within 24 hours of infection. Anemic infarcts in the liver may be present as the result of infection due to either type. Those associated with Type D are generally the more evident. In any case, careful examination is required to locate such infarcts.
Laboratory assistance is frequently required to confirm the diagnosis. Such diagnosis requires the isolation and identification of the causative organism from an area of liver necrosis. The fluorescent antibody (FA) test, although useful, must be interpreted with caution. This test may detect CI. Novyi not responsible for, but which has multiplied following, death of the animal. Further, FA conjugates prepared from CI. Novyi Type B antisera will cross-react with CI. Novyi Type D. Thus, final differentiation may necessitate extensive biochemical and/or toxin identification tests.
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