Abomasal Ulcers in Calves

Robert B Corbett DVM, PAS, Dipl. ACAN ( Dr. Robert Corbett )

By: Robert Corbett, DVM

Abomasal ulcers are defined as a loss of epithelium from the surface of the abomasum, and usually are categorized into four different groups:

  1. Non-perforating with minimal clinical signs
  2. Non-perforating with significant blood loss
  3. Perforating with localized peritonitis
  4. Perforating with acute, diffuse peritonitis

Unfortunately, the majority of the cases that are clinically recognized are type 4, and many are diagnosed at necropsy.  Unless the calves are being closely observed, many of the cases go unrecognized until the ulcer has progressed to a point where successful treatment is difficult.

The healthy abomasum has protective mechanisms in place that help prevent erosion of the mucosal surface.  These include a mucous barrier, bicarbonate, and a high rate of blood flow to the mucosa to provide the necessary nutrients to maintain healthy tissue.  When any of these components are negatively affected, there is an opportunity for the acids normally produced in the abomasum to damage the mucosal epithelium and underlying tissues.

Currently, there is no one definitive cause that has been identified in the etiology of abomasal ulcers.  The cause is usually considered to be multifactorial, so prevention consists of several different management procedures designed to improve the health and integrity of the mucosal surface of the abomasum.  Factors that are considered to contribute to the incidence of abomasal ulcers are: overuse or prolonged use of non-steroidal anti-inflammatory drugs (NSAIDS), corticosteroids, physiological stress, concurrent disease, mineral deficiencies such as copper, quality of milk replacer, feeding frequency, volume of milk per feeding, erratic feeding schedule, osmolality of the milk replacer, poor mixing of the milk replacer, slower abomasal emptying time, type and quality of roughage being fed, trichobezoars, and the presence of certain enteric bacteria such as Clostridium perfringens type A, Campylobacter species, and Helicobacter pylori.

The most common age of milk-fed calves that develop abomasal ulcers is from four to 12 weeks of age.  The majority of the affected calves have ulcers that are subclinical and are not bleeding.  There have been reports of calves being born with abomasal ulcers as well as developing them early and dying from perforated abomasal ulcers within the first few weeks of life.  Some previous studies have suggested that the incidence of abomasal erosions may be as high as 75% of calves, obviously depending on the conditions they are raised under.  The most common time for beef calves to develop abomasal ulcers is from two to four months of age.  A high percentage of these calves will have trichobezoars, but it is not known if they are the underlying cause of the ulcer or if they are the result of the calves licking their abdomens excessively because of pain.

A high percentage of the calves with type 1 ulcers are asymptomatic, and thus difficult to diagnose.  If signs are present, the most common is mild abdominal pain and irregular appetite.  Type 2 ulcers are more obvious since the calves often have tarry black feces and show signs of anemia, along with mild abdominal pain.  Fecal occult blood tests are usually positive if the feces appear to be normal.  Calves with type 3 ulcers are often febrile and partially or totally anorexic. It is common for them to demonstrate abdominal pain.  Disease progression is usually quite rapid in calves with type 4 ulcers.  They show signs of septic shock, rapid heart rate, weak pulse, groaning, severe abdominal pain, dehydration, and cool extremities.  It is common to see abdominal enlargement from the abomasal contents leaking into the abdomen.  Obviously, calves with these clinical signs have a very low chance of survival.

Perhaps the most frustrating part of dealing with abomasal ulcers is trying to determine the underlying cause and what advice to give the owner to reduce the incidence of future cases.  Reducing environmental stress will help reduce blood cortisol levels.  High cortisol levels are associated with an increase in abomasal ulcers.  Animals under stress will have a reduced ability to mount an effective immune response, and it is common for the movement of the gastrointestinal tract to slow down as well.  This creates a problem with slowing down of the abomasal emptying time which is thought to contribute to the formation of abomasal ulcers.  Several studies have shown some association with enteric bacteria and abomasal ulcers as previously mentioned.  The negative effect of cortisol on the animals immune system could also contribute to the growth of these bacteria in the abomasal wall.

The indiscriminate use of NSAIDS will definitely increase the incidence of abomasal ulcers.  Protocols used in the treatment of calves should be reviewed with those responsible for calf care to make sure they are using these drugs in the correct amount and time period specified by the veterinarian.  One study showed that as long as Flunixin Meglumine was used in the correct dosage, there was no increase in the incidence of abomasal ulcers.

Probably the single issue most associated with abomasal ulcers is problems with the feeding process.  The possibilities are numerous but may include the following: inconsistencies in feeding times and volumes of milk per feeding, variation in milk temperature and percent solids, high osmolality of the milk replacer, feeding extremely high volumes of milk, poor quality milk replacer that does not stay in solution or has poor digestibility, feeding only once per day, feeding unpasteurized hospital milk that is high in bacterial numbers, poor hygiene of bottles or buckets used to feed calves or tanks and hoses used to distribute milk, etc. Anything that could result in a lower pH of the abomasum can contribute to the formation of the abomasal ulcer.  One study compared whole milk to all milk-protein milk replacer and soy-protein milk replacer and found that whole milk actually resulted in a significantly lower abomasal pH than did either type of milk replacer, 2.77 versus 3.22 and 3.27 respectively.

Many of the milk feeding programs have become very complicated, especially with computerized feeders.  Amounts fed per feeding, number of feedings allowed per day, total volumes per day are constantly being changed.  It would be preferable to design a program with more consistency, thus allowing the calf to gradually increase its starter consumption while receiving a more constant volume of milk.  Once the calf is eating a sufficient amount of calf starter, the milk can be gradually reduced during the weaning process.

Some studies have shown a relationship between the presence of Clostridium perfringens type A and abomasal ulcers.  As a result, it is generally recommended that herds experiencing issues with abomasal ulcers should vaccinate the calves early in life against this organism.

Some herds have reported an increased incidence in abomasal ulcers while experiencing problems with respiratory disease in young calves.  This is most likely due to stress and higher cortisol levels as well as variations in feed intake.  Once the issue with respiratory disease was corrected, the incidence of abomasal ulcers decreased as well.  Making sure that the calves are healthy should have a positive effect on reducing the incidence of abomasal ulcers.

Oral drugs such as Cimetidine and Ranitidine which are Histamine H2 antagonists, and Omeprazole, which is a proton-pump inhibitor, have shown a significant benefit in the prevention and treatment of abomasal ulcers.  However, unless the animal being treated is extremely valuable, the cost of these drugs is usually prohibitive.  Antacids and protective agents such as aluminum hydroxide and magnesium hydroxide are helpful in producing a transient increase in the pH of the abomasum.

Abomasal ulcers are one of the most frustrating problems that bovine practitioners have to deal with.  However, careful review of the management, environmental conditions, stress factors and feeding procedures will almost always reveal problem areas that can predispose calves to developing abomasal ulcers.  In most situations, the cause is multifactorial and one cannot expect to successfully eliminate the problem simply by changing one thing. Focusing on the areas discussed should allow the practitioner to find possible problem areas, recommend changes, and significantly reduce the economic losses to the client due to abomasal ulcers.


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