Abomasal ulcers in cattle (Proceedings)


Abomasal ulcers in cattle (Proceedings)

Aug 01, 2008


An ulcer is defined as a loss of epithelium from the mucosal surface of the abomasum. The pathologic description, in fact, is an excavation in the mucosa that penetrates through to the muscularis mucosae. This excavation originates from coagulative necrosis. Excavation only partway through the depth of the mucosa is called an erosion. The cause of the excavation is generally due to a breakdown of the gastric mucosal barrier, permitting back diffusion of hydrogen ions. Bile reflux may alter the mucosal barrier as well as non-steroidal anti-inflammatory drugs.1


1. non-perforating
2. non-perforating, bleeding
3. perforating, local peritonitis
4. perforating, diffuse peritonitis


According to the literature, while many calves have been shown to have clinically insignificant ulcers on necropsy, clinically affected calves tend to have type IV ulcers more frequently than any other category. Extensive research has been performed on abomasal ulcers in milk-fed calves. Lesions in calves tend to be located around the pylorus and pyloric antrum. In adults, one study from a referral population examining 69 clinically significant abomasal ulcers on postmortem, found that approximately one-third of these ulcers were type II, while the other two-thirds had types III or IV. Of the cattle with type II, one-half were associated with tumors, wile the other half were not. These tumor associated cases were generally older than 6 years, while the non-tumor associated cases were younger. Of the cattle with perforating ulcers, one-half had local peritonitis and the other half had diffuse peritonitis.2,3 The ventral most portion of the fundic region of the abomasum is a common location of lesions in the adult.4,5,6


There has been extensive research into the etiology of abomasal ulcers in cattle. It is well established that nonsteroidal anti-inflammatory drugs alter the mucosal barrier by interfering with local prostaglandin synthesis. In my experience, as long as an animal is well hydrated and dosed correctly, I have not recognized an induction of an ulcer from therapy with flunixin meglumine. However, that's not to say we should not exercise some caution and discretion in the use of NSAID's. I do believe I've seen cases of abomasal ulcers that were the result, or partially the result of phenylbutazone even at the proper dose. In adults, stress, diets high in starch, concurrent postpartum disease (displaced abomasum, metritis, mastitis, ketosis) and lymphosarcoma have all been incriminated as contributors to the formation of abomasal ulcers. In calves, suckling frequency, route of milk administration (tube vs. suckling), composition of the milk replacer, nature of roughage diet and the presence of enteric bacteria, most notably Clostridium perfringens type A, Campylobacter spp. and Helicobacter pylori have been investigated as possible contributors to disease. 7,8,9 The role of Clostridium perfringens type A, in particular, in the development of abomasal ulcers in calves still remains elusive due to mixed findings. In one study, Clostridium perfringens type A was isolated in 7 of 8 calves diagnosed with abomasitis, and abomasal ulceration, while the remaining calf's abomasum contained Clostridium perfringens type E.7 The same investigators in another study, were able to successfully induce abomasal tympany, abomasitis and abomasal ulceration in 8 calves following intraruminal inoculation.9 However, despite this evidence, one Canadian study found no significant association between isolation of these bacteria and the presence of abomasal ulcer.8

Hairballs in calves have been implicated as well, however, a Canadian study concluded that it was unlikely that the presence of hairballs played a role in the development of fatal perforating ulcers.10 Therefore, the conclusion that can be drawn is that the etiology of abomasal ulcer formation is multi-factoral and intervention/prevention should be aimed at controlling all the factors, which for the most part, should be part of any good herd health program.

Clinical signs

1. Mild abdominal pain – partial anorexia

a. Decreased rumen motility, Ruminal tympany

2. Signs of anemia – pale mucous membranes, tachycardia, tachypnea

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