<br>(User Above)":3ro4a8ll said:: WILL SOME PLEASE TELL ME SOMETHING ABOUT THIS.I'M LOSING 300-400 LB. CALF'S ONE A WEEK.<p><br>Blackleg is an acute, infectious disease cause by Clostridium chauvoei and characterized by inflammation of muscles, severe toxemia and a high mortality. True<br>blackleg is caused by Cl. (feseri) chauvoei, a Gram positive spore-forming, rod-shaped bacterium. The spores are highly resistant to environmental changes and<br>disinfectants and persist in soil for many years. 'False blackleg' may be caused by Cl. septicum and Cl. novyi but this disease is more accurately classified as<br>malignant edema. This indicates that maximum protection to cattle can be provided only by a multivalent vaccine which contains antigens of Cl. chauvoei, Cl. novyi<br>and Cl. septicum. <p>Epidemiology<br>Blackleg is a soil-borne infection but the portal by which the organism enters the body is still in dispute. However, it is presumed that the portal of entry is through the<br>alimentary mucosa after ingestion of contaminated feed. The bacteria may be found in the spleen, liver and alimentary tract of normal animals, and contamination of<br>the soil and pasture may occur from infected feces or decomposition of carcasses of animals dying from the disease. In cattle the disease is largely confined to young<br>stock between the ages of 6 months and 2 years. In the field the disease appears to occur most frequently in rapidly growing cattle on a high plane of nutrition. In<br>Sheep the disease is almost always a wound infection. Infection of skin wounds at shearing and docking and of the navel at birth may cause the development of local<br>lesions. Blackleg is a cause of severe financial loss to cattle raisers in many parts of the world. For the most part, major outbreaks are prevented by vaccination,<br>although outbreaks still occur, occasionally in vaccinated herds, but more frequently in herds where vaccination has been neglected. When the disease occurs it is<br>usual for a number of animals to be affected within the space of a few days. The disease is enzootic in particular areas, especially when they are subject to flooding;<br>such that they may vary in size from a group of farms to an individual field. The case fatality rate in blackleg approaches 100%. <p>Pathogenesis<br>In true blackleg, the stimulus which results in growth of the latent bacterial spores is unknown. Toxin formed by the organism produces a sever necrotizing myositis<br>locally, and a systemic toxemia which is usually fatal. <p>Clinical findings<br>If the animal is observed before death there is marked lameness, usually with pronounced swelling of the upper part of the affected leg. On closer examination the<br>animal will be found to be very depressed, have complete anorexia and ruminal stasis, a high temperature (41°C, 106°F) and pulse rate (100-120/min.). In the early<br>stages the swelling is hot and painful to the touch but soon becomes cold and painless, and edema and emphysema can be felt. The skin is discolored and soon<br>becomes dry and cracked. Although the lesions are usually confined to the upper part of one limb, occasional cases are seen where the lesions are present in other<br>locations such as the base of the tongue, the heart muscle, the diaphragm and psoas muscles, the brisket and udder. Lesions are sometimes present in more than one<br>of these locations in a single animal. The condition develops rapidly and the animal dies quietly 12-36 hours after the appearance of signs. Many animals die without<br>signs having been observed. <p>Necropsy findings<br>Cattle found dead of blackleg are often in characteristic position, lying on the side with the affected hindlimb stuck out stiffly. Bloating and putrefaction occur quickly<br>and bloodstained feces from exudes from the nostrils and anus. Clotting of the blood occurs rapidly. Incision of the affected muscle mass reveals the presence of<br>dark, discolored, swollen tissue with a rancid odor, a metallic sheen on the cut surface and an excess of thin, sanguineous fluid containing bubbles of gas. In some<br>cases the myocardial muscle and diaphragm may be the only tissues affected. All skeletal muscles of the body including those of the lumbar region must be examined<br>for evidence of the lesion, which may be small and escape cursory examination. All body cavities contain excess fluid which contains variable amounts of fibrin and is<br>usually bloodstained. The solid organs show some degree of degeneration, and postmortem decomposition with the production of gas in the liver occurs rapidly. <p>Diagnosis<br>In typical cases of blackleg in cattle a definite diagnosis can be made on the clinical signs and the necropsy findings. However, positive identification on gross<br>postmortem findings of which one of the clostridial myositides is present is hazardous except by an experienced pathologist. This is an important matter if all the<br>common infections are likely to occur in the area. For example, one survey has shown the following isolations from cases of bovine myositis <p> Cl. chauvoei (+ Cl. septicum)<br> 56%<br> Cl. novyi (+ Cl. septicum)<br> 36%<br> Cl. septicum<br> only 6%<br> Cl. sordellii<br> only 1.7%<p><br>In establishing a diagnosis when a number of animals are found dead in a group not kept under close observation one must depend on ones knowledge of local<br>disease incidence, season of the year, age group affected and pasture conditions, and on a close inspection of the environment in which the animals have been<br>maintained. Necropsy findings are most valuable if the cadavers are still fresh but, on many occasions, postmortem decomposition is so advanced that little<br>information can be obtained. <p>Treatment<br>Treatment of affected animals with penicillin is logical if the animal is not moribund but results are generally only fair because of the extensive nature of the lesions.<br>Large doses (10,000 units/kg body weight) should be administered, commencing with crystalline penicillin intravenously and followed by longer-acting preparations<br>some of which should be given into the affected tissue if it is accessible. <p>Control<br>On farms where the disease is enzootic annual vaccination of all cattle between 6 months and 2 years of age should be carried out just prior to the anticipated danger<br>period, usually spring and summer. Vaccination of calves at 3 weeks of age has been recommended when the incidence of the disease is very high. Subsequent<br>revaccination will be advisable . Of the available preparations the formalin-killed, alum-precipitated bacterin is most satisfactory. Immunity does not develop for 14<br>days and deaths may continue for some days if vaccination is carried out during an outbreak. When the disease is present in a group other measures are necessary to<br>protect the remainder of the group until immunity has developed. The constitution of the vaccine is important. A bacterin prepared from a local strain of Cl. chauvoei<br>is preferred. If deaths continue after an approved vaccination program has been used an investigation should be made of the antigenic composition of the vaccine<br>relative to the isolates found in dead vaccinated animals. It is advisable to use a combined bacterin containing Cl. chauvoei, Cl. septicum and Cl. novyi, if these<br>organisms occur in the area and cause clostridial myositis.