The Transition Period Part I: Nutrition and Metabolic Diseases

The transition from non-lactating, late pregnancy to the start of a new lactation can be a troublesome time for dairy cows.  The calving process itself can be a source of problems, suppressing the cow’s immune system, decreasing her appetite, and often causing physical stress or injury.  Lactation demands much more of the cow than pregnancy in terms of energy, protein, and minerals, such as calcium.  Cows are significantly more susceptible to disease in the period surrounding calving, because of the massive metabolic demands of starting milk production.  They are also more prone to infectious disease due to immune suppression and increased potential for contamination at calving.  Infectious disease will be discussed in part II; for now, we focus on nutrition and metabolic diseases.

Milk Fever

Milk fever refers to a sudden decline in blood calcium levels during early lactation.  In late pregnancy, the dry cow has relatively low demands for calcium, much less than is needed to produce milk.  At calving, her body switches gears, pouring massive amounts of calcium into colostrum.  This suddenly increased need cannot be met by diet alone, and so the cow must pull calcium from her own body stores.  If the cow is unable to meet this demand, her blood calcium (which is normally tightly regulated) begins to drop.  Calcium is important for many body processes, but particularly for the contraction of muscles, including the muscles that allow the cow to get up and move, the muscles of her heart, and the muscles that move food through her digestive tract.  Low calcium can make all of these muscles weak.

Clinical Signs: Stage I- Cows with mild decreases in calcium are still able to walk, but will appear restless and may have muscle tremors particularly over the flanks.
Stage II- This is the classic milk fever cow.  She is down and unable to get up, but is sitting up on her chest.  She will often have a low temperature (despite the name milk fever) and cold ears or feet.  Her heart beat is faint and rhythm may be irregular. She often will not eat and may appear bloated, from lack of gastrointestinal motility.
Stage III- Cows in this stage have such severely low calcium that they lay flat out on their sides, unresponsive, severely bloated, and can progress into a coma.  Cows reaching this stage can die if not treated immediately.

Diagnosis:  Cows are often diagnosed based on clinical signs and response to treatment.  However, in certain cases, it is advantageous to take a blood sample prior to treatment.  This way if the cow does not respond to treatment, her blood can be analyzed for calcium levels as well as other minerals or for indicators of other diseases.

Treatment:  Milk fever is treated with calcium supplementation.  Cows in stage I may resolve with oral calcium supplements or calcium given under the skin.  Any milk fever cow that is unable to rise will need calcium in the vein, which must be given slowly so as not to damage her heart.  Some cows may have a concurrent decrease in phosphorus which can be administered in the vein or muscle following calcium administration.  Most cows will be able to rise within two hours of calcium administration, with some getting up immediately.  However, some cases will recover more slowly and may need additional calcium.

Prevention:  Preventing milk fever can be counterintuitive.  It may seem to make sense that we could just add more calcium to the dry cow’s diet, allowing her to store up calcium that she will need for milk.  Unfortunately, the cow’s body doesn’t work this way.  In a time of high supply (a high calcium dry cow diet) and low demand (no milk being produced), the cow will not store up calcium, but rather enter a metabolic state where she is used to excreting lots of calcium in her urine, because there is plenty coming in and little being used up.  Then when she enters lactation, her body, used to calcium in high supply and low demand, suddenly has a very high demand that she can’t keep up with.
So in actuality, our dry cow diet should be low in calcium, activating the cow’s metabolic processes to efficiently absorb and conserve calcium.  Then, when she is switched to a higher calcium fresh cow diet and really needs that calcium, her system is already primed to use it efficiently.  And then we run into another problem: getting calcium low enough while maintaining an otherwise balanced dry cow diet is very difficult and often impractical.
At this point, we have to rely on our knowledge of chemistry to help us.  In short, modifying acid/base balance towards the blood being more acidic prior to calving has a positive effect on calcium absorption and regulation, setting the cow up for more efficient calcium use after freshening.  Acidifying a cow’s diet is done through manipulating the ratio of certain minerals (or adding anionic salts) and should be done in conjunction with a nutritionist as it involves lots of chemical equations and precise calculations.

Another option that is less confusing but more labor intensive would be supplementing all cows with oral calcium upon calving.  For this to work, ideally, cows should receive calcium one day prior to calving and then for 2-3 days post-calving or as a slow release bolus.


In addition to calcium, milk production requires sugars, protein, and fat.  Cows, just like any other animal, get these essential nutrients from their diet.  However, cows are different from animals that eat meat in that they must be able to obtain energy from tough plant material that carnivores would not be able to digest.  Cows have met this challenge by having three additional compartments before their true stomach that allow them to ferment plant material (with the help of bacteria and other organisms that normally live in the rumen) and gain extra nutrients from it.  This means, however, that very few carbohydrates (made up of many sugars bound together) reach the cow’s intestine without being fermented to a different chemical state.  In order to have sugars for milk and as an energy source, cows must make sugar (glucose) in their liver from fermentation products and protein.  Unfortunately, it is not possible to make glucose from fat.
In early lactation, cows have a decreased appetite at the same time that they have much greater energy needs for milk production.  They cannot meet their needs from their diet alone and must start pulling from their own body fat stores.  Fat is mobilized to the liver where it is processed into ketone bodies and sent out for use in other tissues.  However, when glucose levels drop low and large amounts of fat are mobilized, it can overwhelm the cow’s liver leading to ketones building up in the blood stream.  This condition is referred to as ketosis and any disease that decreases the amount a cow eats in early lactation can predispose them to it.  Cows with too much body fat at calving are at higher risk for a large drop in appetite and therefore ketosis.

Clinical Signs: The first signs of ketosis are a gradual loss of appetite and a steady decrease in milk production over several days.  Sometimes, the odor of ketones can be detected on the animals’ breath or in the milk.  Some cows will have neurologic signs such as abnormal licking and chewing behavior, aggression, and increased bellowing.  Cows often have other diseases concurrently (e.g. displaced abomasum, metritis, and mastitis) which may have predisposed her to ketosis or resulted from ketosis.  These cows will have additional clinical signs specific to those diseases.

Diagnosis: Ketones can be measured in the urine or milk with simple strips that change color with ketone level.  If a cow’s liver becomes severely overwhelmed with fat, she can develop fatty liver, a more challenging disease to treat; so, cows that do not respond to treatment or go down should have a full blood chemistry panel run to check for fatty liver and other disease.

Treatment: The goal of treatment is to return glucose levels to normal so the body stops ketone production.  Ketotic cows should be given dextrose (a form of glucose) in the vein.  Dexamethasone is a steroid that affects glucose metabolism increasing the amount in the blood; it can be given with dextrose in the vein or in the muscle.  (Dexamethasone should not be given to pregnant cows, as it can cause abortion.)  Vitamin B12 is vital in the process of making glucose and so this too should be supplemented in the ketotic animal.  Much of the dextrose administered is lost in the urine, and so treatment may need to be repeated so the cow does not relapse.

Propylene glycol is a glucose precursor that can be administered orally to cows as an easily absorbed source of glucose.  This is best for relatively mild cases of ketosis uncomplicated by other diseases.

Prevention: It is unavoidable that high producing dairy cows will enter a state in early lactation where they cannot eat enough to meet the demands of milk production and must pull from their body stores.  Providing a well-balanced diet with plenty of energy will help minimize this effect.  Ensure adequate bunk space, so all cows are able to eat enough.

Other diseases such as milk fever, mastitis, and metritis can decrease a cow’s appetite and predispose her to ketosis; so, preventing these diseases will help prevent ketosis.

Monitoring your fresh cows closely, including use of ketone strips, so you can detect and treat disease early, will help prevent more severe cases.

One of the most important ways to prevent ketosis is making sure that your cows are in adequate body condition at calving.  Dairy cows are body condition scored on a five point scale with a one being a very thin cow and a five an obese cow.  Ideally cows should be between 3.5 and 3.75 at calving.  Too little fat at calving will lead to a quite thin cow in early lactation that will have decreased fertility and trouble recovering her weight.  Too much fat will decrease her appetite at calving mobilize more fat to her liver.  It is essential to observe the cows on your farm, assessing them for body condition and work in conjunction with a nutritionist and/or veterinarian to optimize their nutritional health before entering the metabolically demanding transition period.