Nutritional disorders in finishing beef cattle can result in poor animal health, lowered production efficiency and even animal losses. When we talk about nutritional disorders, a number of conditions spring to mind – acidosis, laminitis, bloat and liver abscesses.

These disorders are all interlinked and are generally associated with (i) feeding highly fermentable feed sources/mainly starch based concentrate diets and (ii) poor feed management.

For finishing cattle, the potential benefits of feeding high-energy diets must be balanced against the risk of digestive disorders.

The problem of acidosis in particular can be addressed through dietary monitoring or dietary modification.

From an overall herd health perspective, the goal should be to minimize the number of cattle that experience acidosis and, for individual animals that experience acidosis, to reduce the duration and intensity of the condition. To achieve this aim, it is critical at farm level that producers are continuously watching and can identify the telltale signs to facilitate early intervention and successful treatment.

Acidosis

Cattle have a digestive system adapted to break down roughage. Bacteria in the rumen break down roughage into energy compounds for growth and maintenance. Most bacteria live in an environment that is close to neutral pH – the typical pH of the rumen on a forage-based diet is six to seven.

Grain is composed mostly of starch and sugars. These starches are broken down rapidly into volatile fatty acids (VFA) and lactic acid. A gradual change in the forage to concentrate ratio of the diet allows the rumen environment time to adapt and the risk of acidosis is low.

However, in an abrupt change to high grain rations, with low effective fibre, the bacteria cannot adapt fast enough to handle such acid conditions. This results in a fall in rumen pH between five and six.

For simplicity, acidosis can be divided into categories of acute or subacute acidosis.

Clinical signs of acute acidosis (pH<5.2) include anorexia, abdominal pain, rapid beating of the heart, diarrhoea, recumbency and death. Cattle that survive the acute acidosis often become “poor doers" due in part to damage of the gastrointestinal tract and reduced absorptive capacity.

Subacute acidosis (SARA; pH 5.6-5.8) occurs more frequently, but is seldom recognised by the producer and is usually of greater economic importance than the clinical disease. The major response by the animal is reduced feed intake with an accompanying reduction in performance.

Acute acidosis and repeated bouts of SARA can damage the surface of the rumen wall. This allows bacteria and toxins to enter blood circulation, potentially causing additional disorders like liver abscesses and an inflammatory response, leading to laminitis problems.

Prevention/treatment

The key to prevention is reducing the amount of readily available carbohydrate consumed at each meal. Ideally, a gradual build-up of concentrates over a three-week acclimation period is recommended.

Along with proper acclimatisation, good diet formulation and excellent feed bunk management are critical to reduce incidences of acidosis. Try to feed the fibre source as close to when the concentrate in fed- stimulate saliva flow. The addition of dietary buffers (sodium bicarbonate) to the diet could also be considered for their perceived positive effects on production and prevention of acidosis.

Treatment of mild cases of acidosis includes withholding concentrate and feeding hay to stimulate saliva flow. Additional therapies include oral treatment with magnesium oxide or sodium bicarbonate (1g/kg body weight initially to alkaline the rumen), along with oral electrolyte solutions.