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.

Swift assassins

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.

A Closer Look: Tips For Managing & Feeding Colostrum

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.

Vaccines

Cows should be vaccinated with a C and D product before calving, and calves at about a month of age. If a herd still experiences problems, Type A vaccine can be added to the program.

If cases occur in calves four weeks or older, they should be vaccinated with a Type C and A product. “I would be especially concerned about Type A, if calves are still having problems at a month or older,” Songer says.

Callan says more veterinarians and producers are using Type A vaccine and feel it helps. Some cases are caused by Type E, however, for which there is no vaccine, he warns.

Autogenous products created from pathology workups on deceased calves are another option. “Some producers have good luck with that approach. Labs can use cultures and generate their own vaccine for a specific organism,” Meyring says.

Thoughts on treatment

When it comes to treatment, the challenge is finding the calf in time. “Many treatments recommended for toxic gut infection are extra-label uses. Producers should discuss treatment with their veterinarian,” Callan says.

Many treatments have been used with success, he adds. “Most important is an antibiotic put into the GI tract where bacteria are proliferating. Veterinarians recommend oral administration of procaine penicillin – a drug effective against all Clostridia – at 1 ml/30 lbs. of bodyweight. Instead of using it according to label directions (injected), it’s given orally,” Callan says.

Some ranchers have good luck saving calves by checking the herd often (at least twice daily), and treating immediately with oral antibiotic (penicillin or neomycin sulfate solution) and castor oil – whenever they find a dull/bloated or colicky calf with severe gut pain. Once the calf goes into shock, however, intensive care with large amounts of intravenous (IV) fluids is crucial.

“Another antibiotic that seems to work is oxytetracycline given at label doses intramuscularly or subcutaneously. It works because some is excreted through the liver into the bile, and into the GI tract,” Callan explains. This drug slows bacterial protein (and toxin) production, and may be effective if given upon first symptoms.

Songer says some producers use a small amount of lasalocid (ionophore) given in a little milk replacer. “You can’t use very much with a calf because it would be toxic, but this ionophore knocks out C. perfringens. Oral amoxicillin or neomycin sulfate would also work,” Songer says. A liquid antibiotic works better and faster in the gut than a pill.

“A single dose of Banamine® helps reduce inflammation, and eases gut pain,” Callan says. “You might also coat the gut lining and protect it from the effects of the toxins with small, frequent doses of Kaopectate® or Pepto-Bismol®,” he says.

“I’ve also heard many times about castor oil as a treatment. Some producers feel it binds/absorbs toxins, and stimulates the stagnant gut to start moving. It’s better than mineral oil, which merely soothes and lubricates.” he says. The usual dose for castor oil is 2-3 oz. for a small calf, up to 5-6 oz. for a two- to three-month-old calf.

“If a calf is bloated, I usually give oil to get things moving and eliminate the toxins – if he’s not so ‘full’ that there’s no room for oil,” Meyring says.

Once a calf goes into shock, however, chance for recovery is greatly reduced. As the calf becomes toxic, the kidneys and liver can shut down, causing toxins to build faster. The calf needs treatment to reverse shock (steroids, epinephrine), along with antibiotics and IV fluids as soon as possible – as much as 5-7 liters – whatever it takes to rehydrate him enough to pass urine again, Meyring says.

Besides combating shock/circulatory failure (by adding volume to the circulatory system and halting the drop in blood pressure), IV fluids also dilute toxins in the blood. Extra fluid helps restore and stimulate kidney function to help remove toxins from the bloodstream. Some veterinarians’ experience in treating toxic calves has shown that if urine production can be restored, most calves survive.

Sidebar: Ulcers are a common aftermath

A calf treated for early signs of toxic gut infection usually does better within hours of receiving oral antibiotic, castor oil and Banamine®. But many calves go off feed a few days later, with low-grade gut pain and ulcer-like symptoms. They grind their teeth, a sign of abdominal discomfort.

“Stomach ulcers, especially abomasal ulcers, are related to C. perfringens infections, mostly Type A,” says Colorado State University DVM Robert Callan. Such calves will quit nursing and, unless force-fed, will go downhill. Some calves have fluid build-up in the abomasum, with sloshing sounds as they move.

“The acute infection can damage the gut lining, which would explain these signs,” says Glenn Songer, Iowa State University Department of Veterinary Microbiology and Preventive Medicine. “We often find abomasal ulceration and necrotic lesions in the lining of the small intestine,” he says.

“Cattle don’t respond to anti-ulcer medications as readily as humans or horses,” Callan says. “To help a calf with ulcers, we give frequent doses of gastric protectants like Kaopectate® or Pepto-Bismol® to coat the gut lining, and try to reduce acid level by frequent feeding. If the calf won’t nurse, force-feed him with small volumes of milk.

“If you can keep the stomach coated and food in it, ulcers eventually heal – usually within a week. The worst thing is when an ulcer keeps eating deeper and perforates the abdomen; then the calf gets peritonitis and dies,” Callan says.

Heather Thomas is a rancher and freelancer based in Salmon, ID.