Source: Manitoba Agriculture Food, and Rural Initiatives
Failure to provide a sound feeding transition program will affect both production and health. Problems during the transition period can result in the loss of 10 – 20 lbs of peak milk, which is equivalent to an economic loss of $400 – $900 per lactation. Metabolic disorders are also more prevalent with an inadequate transition program. These are costly in terms of lost milk production, vet and drugs and discarded milk. Estimates from the U.S. place the economic loss from milk fever at $334, $285 for retained placentas and $145 for ketosis (U.S. dollars).
Occurrence of one metabolic disease also predisposes cows to other metabolic diseases. A U.S. study of 31 dairies during the first 30 days after calving showed significant relationships between various metabolic diseases. Cows with milk fever were 4 times more prone to retained placentas and 24 times more prone to ketosis. Cows with retained placentas were 16 times more prone to ketosis and six times more prone to metritis. Cows with displaced abomasums were 54 times more likely to develop ketosis.
The incidence of these metabolic diseases can be greatly reduced with a good dry cow management and feeding program. This article will look at ketosis, one of these metabolic disorders.
Ketosis and Fatty Livers
Dairy cows rely on glucose for energy. Glucose is produced in the liver from propionic acid, a product of rumen digestion. When DMI is reduced or energy requirements are greater than energy intake, glucose synthesis is inadequate due to insufficient amounts of propionic acid. Alternate sources of energy must be found and body fat stores begin to be broken down. There is also a normal breakdown of body fat around calving time because of the hormonal changes associated with calving. This happens in varying degrees with all transistion cows.
Stress situations also increase mobilization of body fat stores. The breakdown of body fat stores causes the release of nonesterified fatty acids(NEFA). Low energy levels mean the NEFAs are not completely oxidized in the liver. This results in the production of ketone bodies, which cause ketosis, and the increased accumulation of triglycerides in the liver, resulting in fatty liver.
Thin cows have greater mobilization of body fat due to decreased insulin levels and a greater conversion of the resulting NEFAs to triglycerides and ketones.
The liver is not a storage site for body fat but becomes fat as the cow is losing weight. As the amount of fat in the liver increases, liver function is adversely affected. It appears that ketosis occurs after a cow develops a fatty liver.
What We Can Do
- Keep cows on feed prior to calving. A recent study showed that dry cows which went without feed for 8.5 hours between the late night feeding and first morning feeding had significantly higher levels of NEFA than did dry cows who went without feed for only 5 hours. Feed intake was 4.4 lb lower for the group which went without feed for the longest. Ad lib feeding of a TMR or feeding several times daily would be advantageous in pre-fresh and just-fresh cows. Avoid unpalatable feeds.
- Cows should have a BCS of 3.5 to 3.75 at dry-off and calving. If ketosis and fatty livers persist, dry cows off at a BCS one-half condition score lower than usual. This will help to increase feed intake.
- Do not force dry cows to lose weight. Make adjustments in BCS during mid and late lactation.
- Avoid social and environmental stresses. Make any adjustments in location or feeding well before calving – not two to three days before. Provide a well ventilated, clean and well bedded calving stall.
- Feed a well balanced diet to prevent other metabolic problems.
- Lead feed and increase grain as quickly as possible after calving.
- Feeding 6g of niacin per day from 2 weeks pre-calving to 8-12 weeks postcalving may be beneficial.
For further information contact:
Karen Dupchak
Farm Production Extension, Animal Nutritionist
Manitoba Agriculture Food, and Rural Initiatives
204-545 University Crescent
Winnipeg, MB R3T 5S6
Phone: 204-945-7668
Fax: 204-945-4327
