The author is a clinical professor of bovine production medicine at the City University of Hong Kong.

The metabolic disease of ketosis in dairy cattle is more common than is often believed. The formation of ketone bodies is a normal metabolic pathway that occurs in cows, humans, and many other mammals. When the production of ketone bodies gets beyond a certain concentration in blood, that is when the problems appear.

The good news about ketosis is that cows generally respond well to treatment. The bad news is that it has an interesting hereditary component and is highly associated with the presentation of displacement of the abomasum (DA). In fact, cows with blood concentrations of beta-hydroxybuteyrate or BHB (one of the ketone bodies present in the blood) greater than 1.2 mmol/L during the early postpartum period, which is considered subclinical ketosis, are 10 to 15 times more likely to develop a DA.

Leads to other diseases

Subclinical ketosis has also been described as a typical risk factor for other diseases. For example, cows with subclinical ketosis are almost two times more likely to be culled early or die; 1.75 times more likely to develop metritis; 1.52 times more likely to experience retained fetal membranes; 1.61 times more likely to develop clinical mastitis; and two times more likely to develop lameness than cows without subclinical ketosis. Moreover, cows with subclinical ketosis experience reduced fertility, evidenced by lower probabilities of pregnancy after first insemination and longer time to pregnancy.

This is not good for the cow, as we know that a cow with a DA never recovers in milk production, and it is the costliest disease in dairy cattle with values of

$500 to $700 per case. This is why farmers sometimes prefer to send a cow with a DA directly to the slaughterhouse instead of trying any treatment. Surgery is the only

possible solution, but it rarely offers a full recovery of the cow under field conditions.

Having said this, it becomes essential, then, to prevent ketosis or eventually detect cases as early as possible during lactation to avoid the presence of a DA later. For this, it is necessary to know what are the most important risk factors and what can efficiently be manipulated to help prevent ketosis.

Methods to measure

There are many risk factors that are associated with the presentation of subclinical ketosis. Canadian and U.S. studies have determined a concentration between 1.2 to 1.4 mmol/L of BHB as a cut-off value to characterize a cow with this condition. If we manage to have less than 10% of cows with concentrations lower than those mentioned above during the first seven days postpartum, then we can say that the management of the herd is acceptable.

In general, the highest incidence of subclinical ketosis occurs during the first seven days postpartum. In addition, cows that present subclinical ketosis during the first week postpartum are prone to contracting more diseases later, including the feared DA. As a result, then, it is good to start measuring ketone bodies the first four days postpartum.

For this we can use a portable electronic field meter. Each measurement has a cost of $2, but remember that each DA case has an average cost of $600. So, don’t skimp on foolish savings and evaluate ketosis at least once the first week postpartum.

Barriers to prevention

Obese cows during the dry period and at calving is one of the most important risk factors for developing ketosis. Therefore, avoid fat cows at dry off and at calving. Stress is another important risk factor. This causes the cow to begin mobilizing fat excessively and, therefore, develop ketosis. Evade stress, and avoid a high stock density, heat stress, cow movements, and group changes in an unnecessary or poorly done way. In short, offer the best cow comfort and avoid stressful conditions.

Unfortunately, another important risk factor is high milk production related to a high genetic merit for milk yield. This is because a cow selected for greater milk yield also carries genes that are associated with more abdominal adiposity to get energy quicker and excessive fat mobilization, if not managed properly. However, this does not mean that a cow with a high genetic merit to produce milk will always develop ketosis. If the cow is well managed, by providing a balanced diet, along with proper management and comfort, they will be able to express their maximum genetic potential without necessarily suffering from ketosis or other related diseases.

If we manage the herd to have no more than a 10% incidence of subclinical ketosis, then we will be with an acceptable management. Unfortunately, there are many dairy herds in the U.S. that present incidences of ketosis greater than 20% to 25% and therefore experiencing major problems.

Programs to consider

Here are some considerations to keep in mind that come from several studies conducted by researchers at Cornell University.

  1. If your herd has less than 10% incidence of ketosis, identify those cows and treat them individually. One of the most used and successful treatments is to offer 250 to 300 mL (0.4 to 0.6 pints) of propylene glycol orally daily for three consecutive days. Measure ketone bodies again after treatment. If the cow lowers its BHB concentrations to less than 1 mmol/L, it will resume eating normally and recover from subclinical ketosis.
  2. For herds with subclinical ketosis incidences between 15% and 50%, testing cows two days per week from three to nine days postpartum is the most cost-effective strategy.
  3. When herd subclinical ketosis incidences rise above 25%, testing for ketosis and treating cows with propylene glycol is economically beneficial for the farm.
  4. With incidences greater than 50%, treating all postpartum cows with propylene glycol for a period of five days or supplementing powder propylene glycol as top dressing on the TMR during the pre- and postpartum period is the most cost-effective strategy for the herd.
  5. The use of sodium monensin, either as a powder or as slow-release rumen bolus, has also been demonstrated to reduce ketone bodies consistently in dairy cattle. The use of monensin will favor the production of propionic acid in the rumen (the principal precursor of glucose in ruminants), which will contribute to lowering the incidence of subclinical ketosis and related disorders and improve milk production and fertility. Furthermore, monensin can be used as a nutritional strategy to improve body reserves during the dry period in cows dried off with low body condition score that need to calve with proper body condition score.

Ketosis and DAs also occur in grazing dairy cows. In a study we conducted in a grazing herd in Chile, we saw that the annual prevalence of subclinical ketosis using a cut-off value of BHB ≥ 1.1 mmol/L at seven days postpartum was 22.2%. The incidence was higher in cows calving in spring (27%) compared to cows calving in fall (10.3%), and higher in multiparous (24.6%) compared to primiparous cows (15.1%). Milk yield during the first third of lactation was greater in cows with subclinical ketosis compared with cows without the condition; however, disease occurrence was higher in cows with subclinical ketosis and in multiparous cows.

In the end, test for ketosis early in lactation, and treat cows immediately to avoid other diseases, especially displaced abomasum. If your incidence is higher than 25%, consider supplementing the entire prepartum and postpartum herd with propylene glycol and/or monensin.