Rumen Acidosis

Acidosis is said to occur when the pH of the rumen falls to less than 5.5 (normal is 6.5 to 7.0). In many cases the pH can fall even lower.

The fall in pH has two effects. Firstly, the rumen stops moving, becoming atonic. This depresses appetite and production. Secondly, the change in acidity changes the rumen flora, with acid-producing bacteria taking over. They produce more acid, making the acidosis worse. The increased acid is then absorbed through the rumen wall, causing metabolic acidosis, which in severe cases can lead to shock and death.

The primary cause of acidosis is feeding a high level of rapidly digestible carbohydrate, such as barley and other cereals. Acute acidosis, often resulting in death, is most commonly seen in ‘barley beef’ animals where cattle have obtained access to excess feed. In dairy cattle, a milder form, sub-acute acidosis, is seen as a result of feeding increased concentrates compared to forage. It is this form of the disease that NADIS vets have reported increased numbers of.

Clinical Signs

Sub-acute acidosis
Reduced milk yield: Initially a moderate decline, eventually a sudden drop
Milk fat significantly reduced
Body condition and weight loss
Reduction in appetite (initially non-forage feeds)
Dull, stary coat
Reduction in cud-chewing
Mild to moderate diarrhoea
Temperature usually normal
Pulse rate and respiratory rate may rise, particularly if severe.

If acidosis occurs in one cow, it usually indicates that although the other cows in the herd are currently compensating, many are suffering from sub-clinical acidosis that is significantly reducing their productivity. A clinical case is the tip of the iceberg, and therefore solutions have to be for the whole herd not the individual animal.

Many diseases have been linked to acidosis. For some, such as liver abscesses, the evidence is very strong. For others, such as sole ulcer and white-line disease, the link is not so strong.

Diagnosis

Difficult as signs are non-specific
Ketosis (acetonaemia) must be ruled out.

Reduced milk fat is strongly indicative of excess starch feeding
Most diagnoses are based on eliminating other causes of reduced appetite and yield.

Treatment

Most treatment is supportive to allow the rumen to return to normal
Ruminal stimulants are of little value.

Feeding of buffers such as sodium bicarbonate can help in the short term, particularly in animals in the same group.

Prevention

Every treated cow is the tip of the iceberg, so prevention is vital. The aim of any prevention regime is to give the cow time to adapt to change and not to expect the rumen to be able to adapt to whatever is thrown at it.

There are two types of sub-acute acidosis. The first occurs in freshly calved cows (up to 20 days after calving). This occurs because of a failure to adapt the rumen to the lactation diet before calving. In this case, dry cow management is the key to prevention. In particular, feeding a transition diet and minimising calving stress are important.

The second type of acidosis affects cows from peak to mid-lactation. At this time rumen adaptation to the diet should have occurred, so acidosis in these cows occurs as a result of feeding diets that are low in fibre and high in starch (or which allow for feed selection).

In all herds with an acidosis problem there needs to be a full assessment of the feeding, with attention paid to what the cows are being fed and to what they are eating. Each individual situation will be different and require a different range of solutions.

Nevertheless there are several factors which are likely to be of importance in most situations:

Forage to concentrate ratio. Except in very high yielding cows a ratio of 60:40 will significantly reduce the risk of acidosis

Feeding total mixed rations with forage and concentrates mixed can significantly reduce acidosis, provided selection of the concentrate portion doesn’t occur

Feeding space: If there is insufficient space average meal size will increase, increasing the risk of acidosis (even with a TMR). (This can also occur if feeding time is restricted or if feeding times are irregular)

Richard Laven BVetMed PhD MRCVS