Enterotoxemia in baby calves As a rule, doing cow-calf nutrition work is fun. Fun, in that most cow-calf operators have never used a consulting nutritionist, and it's often easy to correct major problems caused by simple deficiencies or imbalances. Either that, or through bidding supplements among manufacturers, you can save cow-calf operators big dollars. The usual result is not only a satisfied client, but more importantly ... you often make a new friend.
Enterotoxemia, however, is where cow-calf nutrition ceases to be fun. I'd say it becomes a headache, except there are cures for headaches. With enterotoxemia in baby calves, there are no easy answers.
As with most cattle diseases, I do my best to pass responsibility to the veterinarian. Unfortunately, the problem here is that applicable research is inadequate. Veterinarians do what they can, but decisions often have to be based on opinions rather than hard data. The result is that we live with enterotoxemia, regardless of what we do to prevent it.
Called "Overeating" Disease The etiology of the disease is that it's essentially nutrition related. The bacteria that cause the disease, Clostridium perfringens (type C and D), are ever-present in the digestive tract of calves. However, the bacteria cannot proliferate and cause a problem unless there are large amounts of nutrient present. Hence, the common name "overeating disease." In that case, the bacteria can multiply rapidly and kill a calf overnight.
This can be a problem for the nutritionist when he begins working with a herd that has had relatively few problems with enterotoxemia, but has low weaning weights and/or poor breedback. Breedback problems are often due to mineral deficiencies or imbalances. Then, you can typically bring conception rates up without any complications.
Breedback can also be due to inadequate energy; and low weaning weights are almost always related to low energy. Increase energy level to the cow and conception will increase, as will milk production and subsequent weaning weight. But, increasing milk flow can also boomerang in the form of enterotoxemia. Get the cows milking well, and suddenly enterotoxemia raises its ugly head.
Taking all precautionary steps, we can still lose 1-3% of newborn calves to enterotoxemia. To be objective, if we raise weaning weights 20 or 30 lbs., or raise breedback 5-10% (in some cases as much as 20%), we can easily afford to accept those losses. However, all objectivity aside, it's disheartening to find what was a bright, frisky baby calf belly up the next day.
Some vets have told clients to vaccinate calves right after birth with C and D vaccine. While that may seem reasonable and prudent, my experience shows it doesn't work. Other vets and immunologists tell me that a baby calf is not able to respond to vaccines for several weeks. My own observations say that is probably correct.
Three weeks seems to be the minimum age at which calves can respond. Indeed, virtually all veterinarians agree that C and D vaccination is mandatory between three and six weeks of age. At that age it provides good protection. (The problem is from three days to three weeks.)
Some veterinarians recommend a prophylactic injection of C and D toxoid at birth, which should give better protection than vaccine. (Toxoid differs from vaccine in that it's comprised of immunity agents taken from the serum of hyperimmunized animals; specific for the toxins produced by the bacteria.) The problem is the expense. If you inject every calf with toxoid, cost wise, there is no advantage over taking some death loss without it. In addition, toxoids carry a label warning for anaphylactic shock. Given that we are only trying to prevent a 1-3% occurrence rate (of enterotoxemia), anaphylactic losses could be a factor. (For extraordinary enterotoxemia losses, prophylactic toxoid injections could be a viable option.)
Most veterinary texts state that the key to prevention is inoculating the cow so she provides passive immunity through colostrum. In theory, that is no doubt correct. The problem is there is an absence of data demonstrating just how effective this is. There are many vaccines that can demonstrate antibodies in the colostrum, but it's unclear how long they provide protection to the calf.
Colostrum production ceases within 36-48 hours and after that any antibodies will have been absorbed into the calf's bloodstream. Certainly while the colostrum is in the calf's gut, protection is provided. The question is after absorption. Can the circulating passive antibodies protect against a massive infection in the gut?
Seeking Feedback From Experts If there are any veterinarians who have research experience in this area, I would appreciate hearing from you. Likewise, if there are vaccine manufacturers who would like to become involved in demonstrations with large herds, I have clients who would probably cooperate.
The bottom line is that enterotoxemia is to cow-calf nutrition work what acidosis is to feedlot nutrition. If you do a good job of grain processing ... some founder and acidosis is inevitable. If you lower gain costs 5-10%, you can accept .5% founders.
But I have never accepted enterotoxemia. It is a bacterial disease and should be preventable. But short of denying the cow the nutrients she needs for meeting milk production requirements, I don't know how to do it.
David P. Price is a consulting nutritionist specializing in feedlot and range cattle. A number of his books and a subscription newsletter are available through BEEF magazine by contacting Marilyn Anderson at 800/722-5334, ext. #710.