The Texas A&M Veterinary Medical Diagnostic Laboratory (TVMDL) has a rich history. Over the 50 plus years we have existed, TVMDL professionals have worked tirelessly to provide the most accurate and up to date resources to our clients. The following excerpt is part of an ongoing series of articles written by TVMDL’s first director, Dr. William Sippel, and other professionals from the earlier days of TVMDL. Some articles were written for features in The Cattleman publication where others were case studies over recent diagnoses. Although much of the content is outdated, Musings from 1 Sippel Road is representation of the progress TVMDL, and others in veterinary diagnostics, have made over the years. Content from this series is not intended to be used to make clinical or diagnostic decisions. We hope you enjoy this look back on TVMDL’s history.
Musings from 1 Sippel Road: Stomach Ulcers in Cattle
By William L. Sippel, VMD
Ulcers in humans are thought to result from nervousness and anxiety. Therefore few people would suspect that stomach ulcers develop in cattle that spend a large amount of their time lying about complacently chewing their cuds. Cattle not only develop stomach ulcers but they have four stomachs in which to develop them.
Ulcers in the rumen, or first stomach, are usually the result of high energy or “hot” ration used in feedlots. These tend to lead to liver abscesses and the ulcer part in the rumen is not itself serious. In the second stomach, or reticulum (“honeycomb”), abrasions, wounds and possibly ulcers may develop due to the lack of selectivity of material swallowed by many cattle. Tacks, nails and other sharp objects often scar the surface of the reticulum or penetrate it and cause so-called “hardware” disease. The third stomach, or omasum (“manypiles” or “dry bible”), can develop ulcerations and I have noted same in cases of organic arsenic poisoning. However, the occurrence of ulcers in the omasum is quite unusual.
True ulceration as described in man occurs in the fourth or true stomach (abomasum) of cattle. Glands in the stomach secrete hydrochloric acid and pepsin which are involved in preliminary digestion of protein in the stomach. With the stomach itself consisting of protein it has long been a puzzle why the stomach does not digest itself. Apparently, it is protected by copius (sp) mucus secretion and probably by substances that inactivate required enzymes. However, the protective mechanism is not completely understood.
Ulceration in cattle usually consists of numerous (20-50) small lesions scattered over different areas of the stomach–although single, large ulcers also occur. The pattern of distribution is characteristic in different age groups of cattle and has prompted several different theories in attempts to explain ulcer development. One such theory is that minute blood vessels supplying many small areas of the stomach lining become plugged by blood clots, thereby causing death and ulceration of the previously nourished area.
Another possible mechanism in formation of ulcers is infection of mechanical scars with fungi or molds that are constantly present. In examining ulcers under the microscope molds have been observed growing down into the tissues and may contribute to the formation of the ulcer. Is is also possible that molds merely invaded the lesion after it already had been formed.
The effect of the nervous system on the formation of ulcers is postulated due to the important nerve and its branches is thought to be another possible cause of ulceration.
Young calves over four weeks of age are most frequently affected with ulcers. It is thought that scratch and other wounds produced by coarse hay and objects damage the lining of the stomach and allow the gastric juices to begin action on the wounds. Ulcers are seldom seen in calves that do not receive roughage. At this young age the rumen is functioning very little, if at all, and most of the food intake goes directly to the abomasum. As a calf gets older, the rumen develops and forage is “softened up” before passing over into the abomasum. These ulcers in young calves usually heal and the calves present no noticeable symptoms. Another suspected cause of rulers is the high acidity of corn silage, which, coupled with other unknown factors, provides enough excess acid to cause development of ulcers in a small percentage of cattle consuming that feed.
Although there are many causes of ulceration of the stomach, the stress of calving appears to be the event with which most ulcers in adult cattle are associated.
Cattle with only a few ulcers may not be visibly ill. On the other hand they may have the appearance of not feeling well and may have tar-like material mixed with their feces.
This material is partially digested blood and its presence or absence depends on the amount of hemorrhage that occurs in the abomasum. Animals with more numerous ulcers that bleed profusely will appear weak, anemic and have definitely tarry stools.
In severe cases where an ulcer penetrates a larger blood vessel and more serious blood loss occurs, the animal will go down, exhibit weakness and pale mucus membrane. It will have a rapid, loud heart rate. At times massive blood clots will be passed in the stool which are similar to those seen in bracken fern poisoning in East Texas cattle in the early summer.
If the ulcer perforates the stomach wall, the stomach content will escape into the abdominal cavity and peritonitis will develop. Sometimes this lesion can be walled off with the momentum or “caul” in the abdominal cavity, but usually the animal develops peritonitis and succumbs. It will exhibit signs of pain in the abdomen. Death usually occurs in less than 24 hours.
Differential diagnosis includes a variety of conditions that produce weakness, recumbency and possibly death along with evidence of blood in the stool. Such conditions include Johne’s disease, parasitism, displaced abomasum, ketosis, lymphoma involving the abomasum (as it frequently does), and bracken fern poisoning. Anaplasmosis causes pallor and weakness but can be differentiated by other symptoms. The usual signs observed are not sufficiently clearcut and characteristic to allow diagnosis of many of these cases.
Treatment is symptomatic and consists of fluids, blood transfusions, antacids and antibiotics. In an unusually valuable animal surgery might be indicated, at least for purposes of visual inspection of the lesion. Surgical removal of the ulcerated area has been accomplished in a few cases that involved a single large ulcer. However, surgery is probably impractical for most ulcer patients as the lesion consists of very numerous small ulcers scattered over a wide area of the stomach.
Stomach ulcers are not a widespread condition nor do they affect more than a few animals at a time; however, knowledge of the condition may explain illness or death in animals exhibiting the above signs.