11 Nov 2019
Figure 2. Abdominal bloat is a usual feature.
Abomasitis is a sporadic disease predominantly affecting neonatal dairy calves younger than three weeks of age, but can be found in any ruminant.
The development of abomasitis is often preceded by abomasal bloat and ulceration. Calf mortality is greater than 60%, with death occurring within six hours in peracute cases or up to two days in less severe instances.
Over the past decade, Veterinary Investigation Diagnosis Analysis (VIDA) figures have shown a rise in preweaned deaths of dairy calves due to abomasitis and bloat. As a percentage of enteric submissions, abomasitis and abomasal bloat have increased from less than 1% in 2008 to nearly 6% in 2017.
In many of these cases, Clostridium species (Clostridium sordellii and Clostridium perfringens) and Sarcina-like bacteria have been identified. Both species are capable of toxin production and rapid fermentation.
Figure 1 shows the submissions of abomasal bloat and abomasitis not otherwise specified, as a percentage of each annual enteric submission (VIDA data). The increase in diagnoses of abomasal bloat and abomasitis from 2008-17 shows a need to address underlying aetiologies and alter management systems to prevent further increases.
Development of bloat and abomasitis can occur rapidly (peracute cases within the first 24 hours of birth), so it is important to note the clinical signs to look out for.
Some clinical signs are common between abomasitis and bloat:
Others can be more specific and depend on the route the pathogenesis takes; abomasitis with or without bloat and ulceration.
The inflammation and organ distention associated with abomasitis leaves the calf with clinical signs associated with pain and discomfort. Others can be more general markers of disease.
Among the more common clinical signs are:
Calves affected in the early stages may present with malaise, reluctance to feed and a depressed state.
As more severe inflammation and ulceration occur, calves may show signs of pain, such as bruxism and bellowing.
Due to the positioning of the abomasum on the ventral right side of the abdomen, severe cases of bloat can be seen as distinct bulging in this area. Reduced gut sounds can be observed and “sloshing” of contents can be heard on manual manipulation (ballottement).
Before abomasitis can develop, the correct environment must be present.
The irritation that leads to abomasitis is caused by toxins produced by Clostridium species and Sarcina-like bacteria. These bacteria require an environment rich in fermentable carbohydrate and a calf with a poor immune status to multiply. If these requirements are met, the pathogenesis takes a predictable and cyclical route – leading to the death of the calf:
If left untreated, the cycle of tissue inflammation and/or bloat, bacterial gas and toxin production will continue until the calf dies.
Five main underlying risk factors appear to exist that enable the establishment of pathology.
Milk replacers form a valuable and easy way of ensuring the calf calorific intake is met. The energy content of milk replacers is significantly higher than that of the equivalent volume of maternal milk, resulting in a high abomasal osmolality.
If the energy content of the replacer exceeds that of the metabolic requirement of the calf, large amounts of easily fermentable carbohydrates will remain in the abomasum. This environment is ideal for the rapid growth of bacteria.
Studies have shown high osmolality inside the abomasum leads to reduced emptying and increased disease occurrence1.
Large volumes can overwhelm the abomasal ability to digest contents and prolong its emptying time.
For low-frequency (once or twice daily) feeding to meet the metabolic requirements of calves, they must provide a higher volume of feed. These high-volume feeds distend the abomasum, slow emptying time and provide ideal carbohydrate-rich environments for pathogenic bacteria to proliferate.
The importance of colostrum cannot be overstated. For a neonatal calf to mount a defence against invading pathogens, it must have sufficient levels of maternal antibodies – in both the lumen of the gastrointestinal tract and the blood2.
For sufficient levels to accumulate in the calf, an ideal concentration of 50g/L of IgG should be present in the dam’s colostrum and the calf must receive sufficient volumes to achieve 10g/L IgG in its bloodstream2.
The rapid movement from milk to milk replacer diet has been linked with the development of abomasitis and bloat.
Milk replacers have high quantities of bioavailable carbohydrates and proteins; while these are important for calf growth, it takes time for the abomasum to adapt to the new diet.
Contamination of feeding tubes, buckets, bedding and other materials increase the likelihood of ingestion of these pathogenic bacteria by the calf.
Other factors that may contribute to the development of abomasitis and bloat include:
Figure 9 is a diagram showing the five most common aetiologies leading to the development of bloat and abomasitis.
Prevention of abomasitis centres on management of the risk factors.
If presented with a sick calf showing the clinical signs of abomasitis, prognosis should be guarded. However, a few steps can be taken to increase a calf’s chances of survival:
Abomasitis and abomasal bloat share common steps in their development:
The five main factors that can predetermine abomasitis are:
