Veterinarians are often faced with determining the cause of death in young dairy and beef calves up to 10 days of age, and giving advice to their clients on what they can do to prevent this from happening. In the majority of cases, the veterinarian does not have the opportunity to observe the clinical signs exhibited by the calf prior to its death. This results in relying upon the observations of the animal owner, and what is observed upon necropsy and subsequent lab diagnostics requested by the veterinarian.
Clostridial organisms are ubiquitous in the environment, and are commonly found in the gastro-intestinal tract of the young calf. For this reason, it is common for the Clostridial organisms to rapidly multiply in the GI tract shortly after death occurs. In order to receive accurate results from laboratory diagnostics, the samples must be taken from a euthanized animal or shortly after death before this overgrowth occurs. An accurate diagnosis is important in determining what management procedures must be implemented to successfully prevent and control the future incidence of this disease.
Clostridial disease can be caused by five different subtypes of Clostridium perfringens: Types A, B, C, D and E. These different types are classified based on the type of lethal exotoxin that they produce. Following is a chart of the five subtypes and the corresponding toxins they produce:
C perfringens Type
Toxin A B C D E
Alpha + + + + +
Beta - + + - -
Epsilon - + - + -
Iota - - - - +
In addition to the exotoxins, C. perfringens may produce two different types of enterotoxins, C. perfringens enterotoxin (CPE) and beta-2 toxin (CPB2). Any of the five subtypes may produce these enterotoxins if the gene is present. These enterotoxins are only produced during the process of sporulation and not by the vegetative bacteria. These toxins may not be present in the intestinal contents if the sporulation process in not occurring. These enterotoxins may increase the severity of the disease but are not necessary for pathogenicity (Simpson et al, Vet Clin Food Anim 34 (2018) 155-184).
Understanding the clinical manifestations of infection by the various subtypes will help the practitioner to come to a more accurate diagnosis of which subtype is most likely causing the problem. Hopefully, the lab results will be definitive enough to confirm the diagnosis.
Clostridium perfringens type A: Even though all of the subtypes have the ability to produce the Alpha toxin, type A usually produces a greater amount than the other subtypes. The amount of Alpha toxin produced varies according to the individual isolate and the subtype. The clinical signs of a type A infection usually are manifested by an abomasitis and/or enteritis in young calves. It is important to understand that the exotoxins can directly affect the tissues where growth of the organism is occurring, and absorption of the toxins into the blood stream is not necessary. Abomasal tympany, with or without abomasal ulceration is common. Necrosis of the abomasal and small intestinal surface may also be present.
Clostridium perfringens type B: The toxin most associated with type B is the Beta toxin. However, Beta toxin is also produced by type C as well. Beta toxin is rapidly destroyed by the enzyme trypsin. Trypsin inhibitors are present in high amounts in colostrum and early milk, so C. perfringens type B infections are not very common in calves that are over two weeks of age. Occasionally, trypsin inhibitors may be present in certain types of feeds which may allow a type B infection in older calves. A hemorrhagic enterocolitis with bloody diarrhea is the most common manifestation of a type B infection.
Clostridium perfringens type C: Type C also produces the Beta toxin so the clinical disease from a type C infection is very similar to the type B. Again, hemorrhagic enterocolitis is the most common result of a type C infection. Type C infections are most common early in life, similar to the type B infections because of the presence of Trypsin inhibitors in the colostrum and early milk.
Clostridium perfringens type D: Type D produces mainly the Epsilon exotoxin. This toxin is rapidly absorbed because of damage caused to the intestinal mucosa and results in enterotoxemia. Unlike Beta toxin, Epsilon toxin requires enzymes such as trypsin to cleave the polypeptide toxin into the active form. It is the third most lethal toxin produced by Clostridial bacteria next to botulism toxin and tetanus toxin. It can produce both local and systemic signs. It causes severe damage to endothelial cells, and as a result, affects multiple organs such as the heart, lung and brain. Since it requires intestinal enzymes to become active, it is not common in young calves because of the presence of trypsin inhibitors. It is much more common in lambs than in calves. If present in calves, they are usually between 1 and 4 months of age.
Clostridium perfringens type E: The Iota toxin is the main exotoxin associated with type E. Like Epsilon toxin, the Iota toxin also requires cleavage by trypsin to be active, and therefore, is uncommon in young calves. This Clostridial infection is quite rare in the United States except for occasional outbreaks in adult goats. A necrotic hemorrhagic enteritis is the most common manifestation of this disease.
It is generally agreed upon that the underlying cause of the majority of Clostridial infections is due to the presence of larger amounts of rapidly available carbohydrate and/or protein that supports the germination of Clostridial spores and subsequent rapid overgrowth of the affected areas of the GI tract. Since Clostridium perfringens is ubiquitous in the environment, the majority of calves will have at least one type of this organism in their GI tract. Slowing down of the GI tract is also thought to contribute to the overgrowth.
Part 2 of this series will focus on management considerations for prevention, including vaccination strategies and feeding programs for calves. The full article, including Part 2, is available online at www.bovinevetonline.com.
Author’s note: A considerable portion of the technical information in this article was summarized from a chapter in the March 2018 edition of Veterinary Clinics: Food Animal Practice, by Simpson, et al, pages 155-184. I would encourage anyone interested in pursuing this topic further to read this excellent summary of “Clostridial Abomasitis and Enteritis in Ruminants”.