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Calf Diarrhea Pathogen Information: Clostridium perfringens, Types C and D

Introduction: Clostridium perfringens is a gram-negative anaerobic bacterium that is divided into subtypes based on toxin production. All subtypes produce alpha toxin. In addition, Type C produces beta toxin and Type D produces epsilon toxin.

Epidemiology:

Type D: Small numbers of Clostridium perfringens type D organisms normally inhabit the intestinal tract of healthy sheep, pigs, deer, cattle, and other species, and do not cause disease. They are common in the feces of healthy animals and in soil. After ingestion, most organisms are destroyed in the rumen and abomasum, and the steady flow of ingesta through the GI tract helps to keep the number of Clostridial organisms in the gut low. When the environment of the gut is changed in certain ways, however, Clostridial bacteria can proliferate and cause disease and death by the production of enterotoxins and subsequent toxemia. High levels of starch in the duodenum due to the grazing of lush pasture or young cereal crops, high levels of grain availability in a feedlot diet, heavy milk feeding, or too much indigestible roughage can cause intestinal stasis and Clostridial proliferation and toxin production. Animals affected by enterotoxemia due to C. Perfringens Type D are generally 1 to 4 months old, in good body condition and on a high plane of nutrition.

Type C: Like C. perfringens Type D, C. perfringens Type C is found worldwide in the environment, the soil, and the feces of healthy animals. Hemorrhagic enterotoxemia due to Cl. Perfringens Type C usually occurs in newborns, as they have a low population of protective normal gut flora and their diet is colostrum, which contains an inhibitor of the Clostridium-destroying digestive enzyme trypsin. Disease due to C. Perfringens Type C is not common, but sporadic outbreaks of severe dysentery with some deaths can occur, especially in calves younger than 10 days of age.

Both types of C. Perfringens form spores and survive for long periods of time in the soil.

Zoonotic risk: Clostridium perfringens Types C and D are not a significant zoonotic concern.

Clinical features/ Specific Therapy:

Type D: The clinical course of enterotoxemia due to C. Perfringens Type D can progress rapidly. Nervous signs frequently predominate; vocalizing, mania, and seizures are followed by death in a few hours in acute cases. In the subacute presentation, calves become docile and blind despite normal blink reflex, and may recover in 2 to 3 days. Calves may suffer peracute enterotoxemia due to C. perfrngens Type D and be found dead with no signs of illness seen before death.

Type C: Calves with disease due to C. perfringens Type C will occasionally die without first having diarrhea. More commonly, they will have diarrhea that may begin as yellow in color and become more brown as the disease becomes increasingly hemorrhagic. Grey or red streaks of necrotic intestinal mucosa may be present in the feces. Calves rapidly become weak, dehydrated, anemic and moribund.

Diagnosis/ Necropsy/ Sampling goals:

Diagnosis of disease due to C. perfringens of Type C or Type D is achieved by isolation of the organism and its enterotoxin from intestinal contents of an affected animal.

Necropsy findings in Type D: Animals with disease caused by Type D are generally in good body condition. Peracute cases may have no gross lesions. More commonly, there may be excess straw colored fluid in the pericardium and thoracic cavity, pulmonary edema, and epicardial and endocardial petechiation. There is patchy congestion of abomasal and intestinal mucosa. This disease is also called “pulpy kidney” due to softening of the kidney caused by renal edema, but this is not a reliable sign on necropsy as autolysis may also cause a softened kidney. Animals dead from C. perfringens Type D may also have glucose in their urine.

Necropsy findings in Type C: C. perfringens Type C results in hemorrhagic enteritis with or without ulceration of gastrointestinal mucosa. There are extensive areas of necrosis in the small intestine, particularly the jejunum, and there may be peritonitis. Mesenteric lymph nodes may be hemorrhagic, and the large intestine may contain blood in the lumen. There may also be subepicardial and subendocardial hemorrhage.

Twenty to thirty milliliters of frozen intestinal contents for toxin isolation plus several air-dries smears for gram stains of intestinal contents should be submitted for analysis. Glucosuria is suggestive of Type D infection. Histopathology of preserved samples of colon, ileum and jejunum may be useful in both types of infection, and analysis of a preserved sample of brain may be useful for identifying Type D infection.

Treatment:

Hyperimmune serum has been suggested as a specific therapy for illness due to either Type C or Type D Clostridium perfringens, but the course of the disease is so rapid that there is very little likelihood of benefit from any therapy begun after clinical signs appear.

Specific Prevention Measures/ Vaccination:

For both types of C. perfringens discussed here, vaccination is inexpensive and effective. Vaccination of the dam against C.perfringens Type C and D, 2 weeks before she calves can help boost colostral protection of the calf. On farms having ongoing problems with Clostridial disease, vaccination should be commenced as colostral protection begins to wane, around the age of 8 weeks, and repeated at 12 and 16 weeks of age. Vaccination at 12 and 16 weeks may be sufficient on other farms.

In the face of an outbreak, animals at risk should be vaccinated and given antitoxin against beta toxin for Type C infection and epsilon toxin for Type D infection. Antioxin is critical in protecting animals at risk, as vaccination with a toxoid is not immediately protective. One dose of epsilon antitoxin will protect a calf for 21 to 29 days, providing plenty of time for vaccination to take effect.

As there is an association between high energy diets and Type D disease, it would be prudent to reduce the energy in rations fed to animals at risk for Type D disease, at least until vaccinal protection can be achieved.

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