What is in this article?:
A how-to on preventing, diagnosing and treating acute toxic gut infections in calves.
Some producers experience frustrating cases of acute enterotoxemia in calves. This term literally means bacterial toxins in the bloodstream generated by bacteria normally found in the intestine. Under certain conditions, these bacteria proliferate rapidly and produce toxins that damage the gut and can kill a calf if not treated quickly.
The most common cause of enterotoxemia in calves is Clostridium perfringens, a Clostridia species that inhabits the gastrointestinal (GI) tract but rarely causes gut infections in adult animals.
Lee Meyring, a DVM in Steamboat Springs, CO, says that despite the availability of good vaccines, many herds still battle toxic gut infection in calves. “We often discover that another genotype is the problem in those herds and have to come up with a different program to try to prevent it,” he says.
The symptoms of toxic gut appear rapidly. One minute the calf appears and acts healthy, then develops sudden gut pain. The calf may quickly develop a distended belly or demonstrate signs of pain – running wildly, then throwing itself to the ground, and kicking and thrashing like a colicky horse. He may get up and down repeatedly on unsteady legs.
The calf soon weakens, and exhibits shock as body temperature and blood pressure drop, gums pale and extremities grow cold. If not reversed quickly, the calf will slip into a coma and die.
The types of C. perfringens that cause disease in cattle include A, B, C, D and E. The most common in nursing-age calves traditionally was Type C, says Glenn Songer, Iowa State University Department of Veterinary Microbiology and Preventive Medicine. “Today, with vaccination of cattle against types C and D, we see fewer C and D infections in calves,” he says.
He says typing of isolates indicates that more than 90% of today’s infections are A, followed by C (4%-5%), and then D. In calves with hemorrhagic enteritis and sudden death, however, E can also be a problem.
“This illustrates the need for diagnostic work to know how to prevent infections. You must go beyond a post-mortem, and do a bacteriologic culture – so you can genotype them and know what you’re dealing with,” Songer says.
According to Robert Callan, a Colorado State University DVM, classic enterotoxemia typically occurs in weaning-age calves, caused by C. perfringens Type D. Clostridia are commonly ingested and inhabit the intestine, but only cause disease if they change from dormant spores into an active, multiplying form that produces toxins. Multiplication can be triggered by an increase in carbohydrates in the diet, such as grain.
“C. perfringens Type D releases several toxins, including Epsilon, which damages the gut wall and is absorbed into the bloodstream. It has adverse effects on cells that line blood vessels throughout the body,” Callan says. Calves will quickly go into shock.
“Vaccination can prevent this disease. Because Epsilon toxin gets into the blood, a calf that already has antibodies against that toxin is well protected,” he adds.
Callan says the other common cause is Type C, which is classically associated with hemorrhagic enterocolitis. This is typically seen in calves less than 14 days old, and is caused by Beta toxin released by Type C.
The reason this occurs in young calves is due to a phenomenon in colostrum. The same factor that enables calves to benefit from antibodies in colostrum makes them vulnerable to Beta toxin.
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Normally, Beta toxin is rapidly degraded by trypsin, an enzyme in the GI tract that breaks down proteins. Trypsin is the natural defense of older animals against Beta toxin.
But colostrum contains trypsin inhibitors, Callan explains. These ensure that colostrum antibodies aren’t rapidly denatured, allowing them to last long enough to get through the gut lining and be absorbed into the blood and lymph, or remain in the gut to fight scour pathogens.
In an older calf, trypsin breaks down Beta toxin and readily destroys it. But trypsin inhibitors in colostrum allow these toxins to flourish.
“If the bacteria multiply swiftly, Beta toxin causes loss of mucosal surface of the GI tract, hemorrhage, rapid progression of disease, shock and death,” Callan says. This is why stockmen vaccinate cows before calving, vaccinate calves at birth, or give newborn calves antitoxin. Some herds experience this deadly disease in very young calves, while others have more problems in calves three weeks to three months of age.
“The best way to prevent disease in very young calves is to vaccinate the dam. Then the antibodies will be in the GI tract as soon as the calf nurses, to neutralize the toxin. When we vaccinate calves at birth, it takes 10-14 days to develop peak antibody levels,” Callan says. Vaccinating calves can be beneficial, however, if herds have problems in older calves.
“Types C and D antitoxin can also be helpful, especially in calves born to unvaccinated dams,” he says. Some ranchers give antitoxin at birth to calves (if they know the dam was unvaccinated or they purchased cows with no vaccination history), or to calves that develop symptoms of disease.
“But we still see herds with calves dying of enterotoxemia, or purple gut disease, because the eight-way vaccine or C and D toxoid were ineffective. When we culture intestinal contents of these calves, there’s often high growth of C. perfringens Type A, and not C or D. Thus, we believe Type A is currently a more common cause,” Callan says.