For high-yielding dairy cows, ketosis has always been the most important metabolic disease. Ketosis can also lead to secondary diseases such as retained placenta, metritis and true stomach displacement. Presently, while veterinarians attach great importance to ketosis in general, subclinical ketosis is often neglected.
1. Classification of ketosis types
Ketosis is caused by cows having inadequate dry matter intake, resulting in their lack of energy to meet maintenance and production needs. Excessive body fat is mobilised beyond the liver's metabolic capacity, leading to an increase in ketone bodies in the blood (beta-hydroxybutyric acid, acetoacetic acid and acetone) and associated disease. Excessive absorption of butyric acid in the rumen can also lead to an increase in blood ketone bodies which directly result in disease.
In this article, according to their etiology, ketosis is divided into Type I, Type II and butyric acid related silage ketosis.
i. Type I ketosis
This ketosis type is typically caused by negative energy balance postpartum. Affected cows are often well managed during the perinatal period, experience normal calving, and show good performance at the beginning of lactation. Subsequently, due to high production levels coupled with insufficient dry matter intake, cows are unable to meet their bodily needs. This leads to mobilisation of body fat, a rise in ketone bodies and associated disease. Type I ketosis occurs mainly three to four weeks after delivery. As the liver is not damaged (in contrast to Type II ketosis), providing adequate glucogenic precursors can alleviate the negative energy balance. The focus on preventing Type I ketosis is on raising postpartum dry matter intake, particularly feed grain, but the risk of acidosis should also be noted. Type I ketosis is relatively easy to treat, with recovery expected within five to seven days.
ii. Type II ketosis
This ketosis type is mainly caused by fatty liver, and typically occurs 12 weeks after delivery. Fatty liver is caused by the accumulation of body fat in the liver when the mobilisation of body fat exceeds the liver's metabolic capacity. Fatty liver damages liver cells, and consequently reduces fat metabolism and gluconeogenesis in the liver. Therefore, once lactation begins, negative energy balance worsens, with fat being increasingly mobilised to form ketone bodies. Research has shown that ketosis is directly related to a reduction in immunity, and directly results in high incidence of infectious diseases (such as mastitis and metritis) one month after delivery. The key to preventing Type II ketosis is in strengthening pre-natal feeding management, maintaining body condition, and reducing obesity in cows. Type II ketosis is difficult to treat and is highly persistent, sometimes up to one month.
iii. Butyric acid silage ketosis
This ketosis type is caused by ketone bodies formed from excessive absorption of butyric acid by the rumen. The excessive butyric acid is mainly a result of feeding poor quality silage. Research has shown that dairy cows consuming more than 50 to 100 grams of butyric acid per day can suffer from ketosis; those that consume more than 200 grams can suffer from severe ketosis.
2. Detection of ketosis
Some forms of ketosis do not show clinical symptoms, particularly subclinical ketosis, and a certain method of detection is required for proper diagnosis. Commonly used clinical tests include blood ketone, urinary ketone, and milk ketone detection.
i. Blood ketone detection
Measuring beta-hydroxybutyric acid content is the gold standard for the detection of ketosis. For healthy adult cows, it is generally regarded that blood concentration of beta-hydroxybutyric acid should be lower than 1.4mmol/L. A concentration of 1.4-3.0mmol/L represents subclinical ketosis, while more than 3.0mmol/L represents clinical ketosis.
ii. Urinary ketone detection
This mainly involves the detection of acetoacetic acid and acetone in urine. Urinary ketone test strips have a sensitivity of about 90%. Due to the relatively low cost of sampling and detection, such tests are suitable for individual cows.
iii. Milk ketone detection
Similar to urinary ketone detection, this mainly involves detecting for acetoacetic acid. Beta-hydroxybutyric acid could also be tested for, but test sensitivity and specificity are relatively low, and the test is less commonly used.
3. Treatment of ketosis
As the fundamental cause of ketosis is negative energy balance, the treatment of ketosis should firstly raise blood sugar concentration, and also increase the provision of glucogenic precursors. There are three main treatment methods:
i. Glucose delivery through intravenous injection to rapidly raise blood sugar levels and stimulate insulin secretion
Glucose delivered through intravenous injection is retained in the blood for only two to three hours. For clinical ketosis, treatment dosage is 500mL of 50% glucose, administered every four to six hours for severe ketosis (with neurologic signs), and just once for less severe forms of the disease.
ii. Oral administration of glucogenic precursors, mainly propylene glycol, glycerol and calcium propionate
Propylene glycol is directly absorbed through the rumen wall and converted by the liver into sugar. In general, the therapeutic dose is 500ml per day, administered for three to five days. As propylene glycol has poor palatability, its administration is recommended after feeding.
iii. Dexamethasone injection
Dexamethasone can increase glucose production for a period of two to four days, but carries the risk of immunosuppression and abortion. For clinical ketosis, a single dosage is recommended five to 50 days postpartum. As for subclinical ketosis, the administration of glucogenic precursors instead is typically sufficient.
4. Prevention of ketosis
Basic prevention of ketosis involves avoiding an excessive drop in feed intake prepartum, reducing body fat mobilisation, increasing postpartum feed intake, and reducing the degree and period of negative energy balance.
Vigilance is required when dry matter intake falls below 12 kilograms during the perinatal period. Research has shown that using the same feed ingredients before and after delivery helps in the recovery of feed intake. Management of the calving area is also very important. Providing cows with ample calving space, feed and water, and maintaining environmental comfort, can reduce stress during the calving period. Other aspects of management include preventing temperature stresses, maintaining hygiene levels in the drinking and feeding troughs and play areas, and strengthening disinfection protocols. Body condition should also be maintained, and obesity avoided.
As niacin is involved in fat metabolism, administering niacin can effectively reduce incidence of ketosis. Before delivery, the recommended dosage per cow is six to 10 grams per day. Administration can be continued post-delivery.
On a daily basis, administer 60 grams of bypass choline to each cow for a period of 30 days before and after delivery. Choline can increase the level of very low density lipoproteins which transport triglycerides.
During the dry period, administer monensin. Monesin can inhibit Gram-positive bacteria, and increase propionic acid production in the rumen which reduces fatty liver and ketosis.
Ketosis has become an important factor affecting dairy herd health. Dairy farm managers and veterinarians should strengthen their emphasis on ketosis, particularly the monitoring and prevention of subclinical ketosis.
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Article made possible through the contribution of LI An-ming, DVM, staff writer at eFeedLink