Calving season is over. You're casually checking cows on a Sunday when you notice a cow at the herd's edge with no calf in sight and a tight bag. As you approach her, she moves to a different part of the pasture where you find her dead 250-lb. calf.
With no evident cause of death, you call your veterinarian. "Doc" gives you a list of possibilities - blackleg, lightning strike, pneumonia and abomasal ulcers.
Abomasal ulcers result when the lining of the calf stomach is eroded in small focal areas. Calves diagnosed with abomasal ulcers are typically found dead. A necropsy will reveal a perforated ulcer in the abomasum or upper part of the small intestine and usually widespread peritonitis.
In cases where the animal is alive, symptoms may include kicking at the belly, frequent lying down, a distended abdomen, perhaps sunken eyes (evidence of dehydration) and even increased rectal temperatures. Animals with mild symptoms will not show dehydration and increased rectal temperatures.
Diagnosis of this condition in the live animal depends on the age of the animal (2 to 4 months), signs and symptoms of the disease and response to therapy. Therapy includes broad-spectrum oral antibiotics and kaolin pectin.
Not A New Problem Studies were published 72 years ago that reported 78-98% of 4- to 14-week-old calves were affected by abomasal erosion and/or ulcers. We've made little progress in determining the conditions' true prevalence in our calves, the risk factors and/or causes.
The abomasal ulcers that get our attention are those that become severe to the point where the stomach is perforated, which results in local or diffuse peritonitis (infection and inflammation of the abdomen). Once peritonitis has developed, successful treatment is very difficult.
We don't have a good estimate of the prevalence of non-fatal and fatal abomasal ulcers. However, the limited data in calves and data from other species suggest that non-fatal abomasal ulcers are common.
Determining the prevalence of non-fatal abomasal ulcers would require examining the stomachs of large numbers of calves with an endoscope. Determining the prevalence of fatal abomasal ulcers requires a gross postmortem exam, which is rarely done on many farms and ranches.
The 1992 NAHMS Cow/Calf Health and Productivity Audit lists "unknown" as the second most common cause of calf death. Perhaps all these are abomasal ulcers, maybe none of them.
But, it follows that if we don't know the prevalence, we have limited understanding of the risk factors/causes. So, the definitive cause(s) of abomasal ulcers in calves remain murky. Our ability to evaluate the effectiveness of intervention strategies also is severely hampered.
In recent years, significant advances have been made in our understanding of gastric ulcers in other species. Recently, the relationship between the bacteria Helicobacter pylori, probably acquired early in life, and gastric ulcers in humans has been described. Following this have been reports of the therapeutic success of antibiotics, along with other medications that reduce acid production, in treating gastric ulcers.
Other Species Offer Insight Studies in young horses reveal a 50-100% prevalence of gastric ulcers. Studies in pigs show 5-100% (average 28.5%) of pigs have gastric ulcers. It's not known if these results are directly relevant to abomasal ulcers in beef calves, but it's food for thought.
In calves, bacterial agents such as Helicobacter pylori, Clostridium perfringens, Campylobacter spp., and streptococci, as well as fungi, have been implicated. However, a study in Canada failed to show an association between these and ulcers. Several other reports implicate Clostridium perfringens as a risk factor.
The mixed evidence on infection and abomasal ulcers doesn't mean bacteria aren't involved, but it does imply other factors are important in ulcer development. Some of the factors include trace mineral imbalances, hairballs and stress.
Trace mineral deficiencies such as copper and selenium have been implicated in Nebraska and Wyoming. Copper has been shown to be involved in prostaglandin synthesis, and certain prostaglandins are very important in preserving the integrity of the inner lining of the abomasum.
In other species, including humans, stress has been shown to have a role in the development of ulcers. It's difficult to appreciate the role of stress in suckling calves on pasture, but anecdotally it appears that rapidly growing calves on lush pasture with high milk intakes are more predisposed to abomasal ulcers and perhaps physiological stress is important.
Because the cause of this condition isn't completely known and few animals within a herd show symptoms or die from this condition, designing prevention strategies is difficult. A few recommendations can be made, but the effectiveness of any of these is questionable.
* Assess trace mineral supplementation, particularly copper. This might include assessing sulfur and molybdenum levels in the diet and water. Liver biopsy for copper in a percentage of animals may be necessary.
* Vaccinate young calves for clostridial infections, including Clostridium perfringens.
* Reduce stressors.
Until we take a large-scale, scientific approach to this condition, it's unlikely we will advance much beyond where we have come in the last 72 years - vague recommendations based on theory and continued frustration.
Louis Perino, DVM, PhD, is a professor of immunology, health and management at West Texas A&M University in Canyon. Gerald Stokka, DVM, MS, is an associate professor and Extension beef veterinarian at Kansas State University in Manhattan.