F120
Clostridial Diseases

blackleg | malignant edema | black disease | black neck | red water disease | entertoxemia (neonatal hemorrhagic enterotoxemia) | entertoxemia (overeating disease and pulpy kidney disease) | tetanus | botulism (forage poisoning)

Causative Agent: This disease most commonly affects cattle under 2 years of age. It is caused by a soilborne bacterium called Clostridium chauvoei.

Clinical Signs: The most common sign is sudden death. Often, the disease develops so rapidly that death can occur before the owner has noticed any sickness in the herd. Other signs are lameness, lethargy, fever, and swellings that appear in various muscles of the body. In the later stages of the disease, these swellings spread and gas forms under the skin, producing a crackling sound when pressed with the hand.

Disease Transmission: The disease is spread by ingesting the bacteria. The bacteria then enter the blood stream and spread to the muscles and tissues.

Diagnosis: A necropsy examination of the affected animal reveals areas of black dead (necrotic) muscle that has pockets of gas bubbles. Specimens of affected muscle tissue must be sent to a laboratory as soon as possible for confirmation of the disease.

Treatment: If the disease is identified in the early stages of infection, animals may respond to immediate treatment with large doses of penicillin or other antibiotics.

Prevention: Prevention is accomplished by using blackleg vaccines.

Causative Agent: This disease is caused by the bacterium Clostridium septicum. It is found in animals of all ages, but is more common in older animals. The disease is very similar to blackleg.

Clinical Signs: Some signs of disease are lethargy, loss of appetite, and a wet, doughy swelling around a wound, which can gravitate to lower portions of the body such as the belly wall or lower limbs. High fevers are associated with the infection, and death frequently occurs within 24 to 48 hours.

Disease Transmission: The organism often enters the body through puncture wounds or injuries contaminated by soil or feces that contain the bacteria; it can even be introduced through deep vaginal or uterine wounds following a difficult birth.

Diagnosis: Necropsy lesions are usually wet, darkened, foul smelling areas under the skin, often extending into muscle. Unlike blackleg, very little gas, if any, is associated with these swellings. Laboratory confirmation is required for a final diagnosis.

Treatment: Occasionally, if the condition is noted early, treatment with high doses of penicillin is successful.

Prevention: Vaccination and boosters using a combination vaccine are the best prevention.

Clinical Signs: Animals sick with this disease normally do not show signs of infection. Sudden death is often the first indication that there is a problem.

Disease Transmission: The route of infection is unknown; however, it is thought to gain entrance into the body by wound infection or ingested by mouth.

Diagnosis: Necropsy lesions (wet and foul smelling) are similar to those seen in malignant edema. Laboratory confirmation on affected tissue is required for an accurate diagnosis.

Prevention: Vaccination and boosters using a combination 8-way vaccine are the best prevention.

Causative Agent: This disease, found primarily in feedlot cattle, is caused by Clostridium sordellii and causes sudden death.

Clinical Signs: Clinical signs are usually not observed, due to the sudden death of most infected animals.

Disease Transmission: The route of transmission is unknown, but is thought to be by ingesting the organism.

Treatment: No treatment is currently available.

Prevention: Vaccination and boosters using a combination 8-way vaccine are the best prevention.

Causative Agent: Clostridium haemolyticum causes this infection. This disease is somewhat limited geographically and is associated primarily with marshy lowlands.

Clinical Signs: Some signs of infection are lethargy, anemia, bloody diarrhea, red-stained urine, fever, collapse, and death in 1 to 3 days. The disease was named red water because of the red colored urine in the infected animal.

Disease Transmission: This organism is taken in by mouth when contaminated soil is ingested. Disease is often associated with liver flukes that damage the liver allowing the bacteria to proliferate.

Diagnosis: A necropsy finds an extremely pale (anemic) animal, red-stained urine in the bladder, thin/watery blood, and usually a large, dark area of dead tissue in the liver. Laboratory testing is required to confirm the diagnosis.

Treatment: Treatment is of no value unless it is begun in the early stages with large doses of penicillin.

Prevention: Vaccination and boosters using a combination vaccine are the best prevention. More frequent vaccination may be necessary in heavily infected areas.

Causative Agent: This type of enterotoxemia is caused by Clostridium perfringens type C. This organism is found in the intestines of humans and animals throughout the world. Enterotoxemia occurs in animals of all ages (particularly calves < 1 month) when feces containing the bacteria enters the mouth. This often occurs when contaminated hands and equipment are used on newborns.

Clinical Signs: Young animals refuse to nurse and show signs of lethargy, abdominal pain, convulsions, and diarrhea. The diarrhea may be yellow, brown, and/or bloody. Many young animals die before signs are even noticed.

Prevention: The disease is best controlled by vaccinating the pregnant mothers during the last third of pregnancy.

Clinical Signs: An abrupt death of an apparently healthy animal is often the first sign. In some cases, excitement, circling, incoordination, and diarrhea are seen. Adult animals may show the same signs, with death occurring within 24 hours.

Disease Transmission: C. perfringens normally lives in the intestinal tracts of almost all animals. For overgrowth of this organism to occur, there must be an abundance of nutrients present in the gut, especially carbohydrates like those found in milk and grain. There must also be a slowing of intestinal tract movement caused by ingesting a particularly large amount of feed. This allows the C. perfringens to overgrow, accumulate, and be absorbed from the gut.

Diagnosis: Necropsy shows possible lesions on sections of the small intestine and kidneys. A blood tinged, thick fluid is sometimes found when the gut is opened. Hemorrhages may be found on the heart and thymus as well. An exact (definitive) diagnosis can be made in the laboratory from a refrigerated sample of gut fluid that was collected under sterile conditions.

Treatment/Prevention: Treatment is difficult once signs of illness begin, so the best method of control is prevention. Prevention includes vaccinating all breeding females twice in their first year and then boostering them again each year 3-6 weeks before giving birth. All calves should be vaccinated at 6-8 weeks and then boostered again 3-4 weeks later. Reducing the amount of grain (concentrate) in the diet can also help.

Clinical Signs: At first, the animal shows signs of stiffness in the head and neck region and the inability to move in the hind end. The muscles of the mouth, head, and neck become extremely stiff (lockjaw) and often spasm. As the disease progresses, the animal has difficulty turning, backing, and eating. Death occurs in approximately 80% of the non-protected animals.

1. Prevent additional spread of the toxin in the animal.
   1. Administer 3.3 mLs of procaine penicillin G per 100 lbs., intramuscularly (IM), twice a day. Inject some of the antibiotic around/in the injured area.
   2. It is also necessary to administer 10,000 - 50,000 IU (International Units) of tetanus antitoxin, IM.
2. Provide supportive care.
   1. Because the animal has little to no muscle control, provide areas with good footing.
   2. Provide plenty of water and food that is easily accessible.
   3. Supply plenty of straw and soft bedding to prevent sores, since the animal may spend much of its time down.
3. Establish protection in the future.
   1. Give a tetanus toxoid shot, and booster it again in one month.

Causative Agent: Botulism is caused by the toxin from the bacterium Clostridium botulinum.

Clinical Signs: Signs of botulism may include muscle paralysis, weakness, and ataxia. Problems with the mouth including difficulty chewing and swallowing also occur. The jaw may hang open and tongue protrude out of the mouth. The head is sometimes turned back against the flank and the cow may go completely down. Botulism may cause bloating, constipation, and decreased rumen contractions. Death can occur within 24 hours of clinical signs and usually is the result of respiratory or heart failure. If the animal survives, it may experience weakness that can last for weeks.

Disease Transmission: This organism or preformed toxin enters the animal’s body either by ingestion or through a wound. Contaminated feed, pasture, silage, and animal carcasses can be sources of infection.

Diagnosis: A diagnosis of botulism can be made if the toxin is found in blood (serum), food, or gut samples. Sometimes, the organism can be cultured from the feed. Necropsy findings are not usually helpful in specifically diagnosing this problem.

Treatment: Treatment includes fluids and nutritional support. If the infection is caught early or is thought to be caused by wound contamination, antibiotics may be administered. An antitoxin is also available that can help in animals that are in the early and mid-stages of the disease.

Prevention/Control: Cases of botulism can be controlled if good management practices are implemented. These include disposing of dead carcasses promptly and never feeding spoiled feedstuffs or silage.

Summary: Clostridial diseases present challenging problems to diagnose, but can often be effectively controlled with proper vaccination programs. Producers should work very closely with a local veterinarian to set up programs for prevention of the common clostridial diseases in the area. Prompt necropsy examinations and tissue collection for laboratory testing are important for an accurate diagnosis and to prevent additional cases in the future.