Metabolic Diseases - The Symptoms of a Greater Problem?

Steve Radostits

Leduc Veterinary Hospital Ltd.,
P.O. Box 3419,
Leduc, AB, Canada T9E 6M2

Take Home Messages

Most metabolic diseases occur during the period commencing at calving and ending at the peak of lactation. Therefore the feeding and management of the close-up dry cow and the fresh cow are the key to prevention.

The dry cow period is not a rest phase, but rather a preparatory phase. Prepare for a trouble free, PROFITABLE, lactation by implementing carefully balanced far-away and close-up dry cow rations.

Feed cows according to milk production AND body condition. Do not attempt to make body condition adjustments during the dry period.

With metabolic disease there is usually a broken management system so ... Fix the cow today and rebuild the management system tomorrow to prevent new cases.

Introduction

Metabolic disease occurs when there is an imbalance between the rates of input of dietary nutrients and the "output" of production. The most common metabolic diseases would include ketosis, milk fever, and the fat cow syndrome. The incidence of metabolic disease in the dairy cow is highest during the period commencing at calving and ending at the peak of lactation. The high producing cow is always on the verge of abnormality during this critical time she is "red lining it". The rapid exchange of water, electrolytes, and energy that occurs during early lactation makes the cow vulnerable to "crashing" if abnormalities in INPUT due to changes in dry matter intake (DMI), digestion, or absorbtion take place. The same applies if there is a sudden change in the OUTPUT of these nutrients whether it occurs through secretions into the milk or excretions by other routes. Feeding practices during the dry period and early lactation are critical for the maintenance of a healthy balance between the inputs and outputs that occur during this period of time. The goal is to provide a healthy balance, a comfortable cow, and a low level of metabolic disease.

Ketosis

Introduction

Ketosis is a condition that can occur when the output of energy is greater than the input over a period of time. The net result is an energy deficiency. The cow attempts to reduce the impact of this deficiency by mobilizing large amounts of her own body fat so that it can be transported to the liver and converted into energy. When this occurs at an accelerated rate the liver's capacity to process it is exceeded and ketones rather than glucose are produced.

The incidence of clinical ketosis in Canadian dairy herds from two studies was 3.3 to 7.4%(1, 5). Problem herds can be as high as 40%. The goal should be to have ketosis in less than 3% of the fresh cows annually (9). Ketosis is considered to be one of the major causes of loss to a dairy farmer because of both decreased production while the disease is present, and the failure of the cow to return to full production after recovery.

Most cases of ketosis occur in the first 30 days after calving with 90% of the cases occurring by day 60 (7). It would be rare for a dairy cow with reasonable lactation potential not to be in a net energy deficiency post-calving. This occurs because milk production peaks approximately 8 to 10 weeks after calving and DMI does not reach a maximum until 10 to 12 weeks. In fact 12 to 34% of fresh cows may have subclinical ketosis because the output of energy is exceeding the input and the capacity of the liver to convert body fat to energy is being challenged (3). These cows are "on the edge" and a small change in nutrition or metabolism may push them into the clinical category.

Definitions

Primary Ketosis. The diagnosis of primary ketosis implies that there is no other disease process present that may have contributed to a net energy deficiency. It occurs in cows that are in good to excessive body condition that have good production and are being fed a good quality diet. The risk factors associated with primary ketosis include:

excessive body condition at calving,

rations with inappropriate protein/energy levels ,

extended dry periods, and

inadequate exercise.

Secondary Ketosis. Secondary ketosis occurs when some other disease such as milk fever, mastitis, metritis, ruminal acidosis, or a displaced abomasum contributes to a decreased energy intake and pushes the cow into clinical ketosis.

Clinical Signs

Clinical. Wasting Form. This is the most common form of the disease. There is a gradual decrease in appetite and milk production over two to four days. Cows usually decrease their intake of grain first. They will usually continue to eat some hay unless the ketosis becomes severe. There is a RAPID loss of body condition. Ketones can be detected in their breath and a positive urine ketone test confirms the diagnosis.

Nervous Form. This form of the disease has a sudden onset and is characterized by bizarre nervous signs. The animals are usually delirious and will walk in circles, lean into stanchions or tie bars, lick pipes, appear to be blind, and often are constantly chewing with profuse salivation. When they walk they have an unsteady gait.

Subclinical. The subclinical form is much less dramatic of course because it is not immediately obvious. However it can have considerable economic impact on a herd because it can decrease milk production by 1 to 1.5 kg/day (4), and decrease fertility (8, 12).

Control and Prevention

Avoid overconditioning cows in late lactation. Strive to have fresh cows calving with a body condition of 3.0 to 3.5.

Do not attempt to alter body condition during the dry period. There should neither be a gain or a loss of condition during this time.

In early lactation avoid diets that are too high in protein. Excess levels of both degradable and undegradable (max. 40%) CP have been associated with an increased incidence of ketosis.

Avoid diets too high in carbohydrates or too low in fiber such that ruminal acidosis is present. Total ADF in the ration should be 19 to 21%. Make sure adequate functional fiber is present as well should have 30% of forage (by weight) greater than 1 cm in length and 15% greater than 4 cm in length. In component fed herds increase grain gradually (0.5 kg/day) to prevent acidosis and secondary ketosis.

The use of fats such as tallow and oils such as canola oil should be used to increase the energy available in the ration.

Implement a close-up dry cow ration where cows are lead-fed two to three weeks prior to their due date. Cows should be started at approximately 1 kg of grain and be eating 3 to 4 kg at the end of the two to three week period. Cows should be introduced to the forage they will be fed in early lactation at this time as well.

Feed your best quality forage to the fresh cows because it will likely have the highest energy values.

Provide exercise to housed cows at least one hour per day.

Do not feed silage exclusively feed some hay (2.5 kg ) if possible. This will help to prevent ruminal acidosis and secondary ketosis.

Fat Cow Syndrome

Introduction

Mild fatty infiltration of the liver is common in high-producing dairy cows at or near the time of calving. The underlying problem is an energy deficiency. The input of energy through feed intake/digestion/absorbtion is less than the output of energy into the developing calf and the production of milk. This deficiency causes the cow to mobilize her own fat stores in an effort to make up the deficit. The fat goes to the liver to be processed. If this happens at an accelerated rate both the liver and muscle are infiltrated with excessive amounts of fat. In severe cases this causes structural damage to the liver which causes anorexia and depression. Severe infiltration of muscle tissue with fat may be related to the weakness and recumbency seen in severe cases of this disease. In severe cases the liver fails due to the structural damage caused by the invasion of excessive amounts of fat. Once liver failure is present the animals become weak, recumbent, and die within one or two days.

Clinical Signs

Mild. A mild case of fat cow syndrome or fatty liver will usually look very much like a case of primary or secondary ketosis. Clinically it would not be possible to differentiate between the two diseases. These cases should respond to aggressive therapy which would include intravenous dextrose, steroids, and oral propylene glycol.

Severe. Severe cases of fatty liver will often occur within the first few days after calving (11). There is often a history of some other disease such as milk fever, ketosis, retained placenta, mastitis, or a displaced abomasum at the time of calving. The animal does not respond completely to the routine treatments for these diseases. They usually go right off feed and develop a severe ketosis. Within a few days they may not be able to stand and death can occur in 7 to 10 days despite aggressive treatment.

Control and Prevention

Prevent excess body condition gains in late lactation. The use of a body condition scoring system at strategic times throughout lactation will help to achieve this goal. An example of such a program would be to score cows at 120 days prior to dry off, at dry off, at calving, 40 days in milk, and at 100 to 120 days in milk. Many of the software systems in place on our western Canadian dairies can be programmed to generate such an action list. Changes in feeding can than take place based on the scores. It is also quite useful to graph the scores so that you can get an impression of what the herd is doing at these different times. Cows need to be fed based on milk production AND body condition.

Prevent extended dry periods. Often these are the result of poor conception rates and therefore extended lactations and dry periods. Breeding problems should be investigated if they are the root of these extended dry periods and lactations.

Treat high risk cows with oral propylene glycol prophylactically until they are eating aggressively. For example high risk cows can be treated with 250 ml of propylene glycol once daily as an oral drench for the first 7 to 10 days after calving.

Treat postpartum diseases such as milk fever, mastitis, retained placenta, and ketosis promptly in order to prevent severe fatty infiltration of the liver.

Perhaps the use of BST (bovine somatotropin) will help us prevent excessive body condition gains in late lactation. This could potentially be a useful tool for those cows which have had breeding problems and are putting on excessive amounts of condition in late lactation.

Milk Fever

Introduction

Milk fever is a metabolic disease that most commonly occurs in cows shortly before or after calving. It is characterized by inappetence, weakness, depression, and eventually recumbency. The disease is a result of depressed blood calcium levels. It is similar to other metabolic diseases in that once again the output exceeds the input and a clinical syndrome develops. Calcium plays an important role in muscle contraction as well as the transmission of nerve "messages" to the muscle fibers. Thus when blood calcium levels are depleted abnormalities such as muscle tremors, and in more severe cases complete lack of muscle tone causing recumbency, can occur.

The onset of lactation results in a sudden demand on available calcium. To illustrate the magnitude of this demand consider that the production of 10 kg of colostrum requires 23 grams of calcium. This represents nine times the amount normally present in the blood. Therefore the cow has to increase her blood calcium levels significantly to meet this increased demand. She accomplishes this by increasing the amount of calcium absorbed from the intestinal tract and by "stealing" some from her bone reserves. Cows which cannot adapt to this sudden change develop a state of hypocalcemia with severe cases developing the classical signs of milk fever. Recently there has been increased interest in subclinical hypocalcemia. This can affect up to 50% of the animals in some herds (11). This syndrome occurs when an incomplete adaptation to the increased calcium demand occurs and it can persists for the first few weeks of lactation. The significance of this syndrome is that it results in decreased rumen motility which will decrease appetite and exacerbate the negative energy balance that already exists in the fresh cow.

Risk Factors

The incidence of milk fever varies from farm to farm. Few figures are available for Canadian herds. In the U.K. rates of 3.5 to 8.8% of susceptible cows have been recorded (11). On individual farms the incidence can be as high as 25 to 30%. The goal would be to have less than 5% of fresh cows develop clinical milk fever (3). The risk factors considered most influential in this disease are the age of the cow, high milk production, and the close-up dry cow ration.

Age. As cows age their production increases and therefore the calcium demand at the onset of lactation also increases significantly. Unfortunately the cow's ability to "steal" calcium from bone reserves diminishes as she ages. In addition their ability to absorb calcium from the digestive tract becomes less efficient. As a result older high producing cows can have a difficult time adapting to the onset of lactation. Most cases of clinical milk fever are seen in cows in their third lactation or greater.

Production. Cows with high milk production must transfer a higher absolute amount of calcium into milk. This increases the risk of developing both subclinical and clinical milk fever.

Close-up Dry Cow Ration. There are several factors within the close-up dry cow ration that will affect the incidence of milk fever.

Calcium. There have been many studies done on the effects of the absolute and relative amounts of calcium and phosphorous in the diet. Feeding greater than 100 g of calcium daily has been associated with an increased incidence of milk fever (2). When a cow is fed greater than 100 g of calcium per day her needs are met by passive absorption of calcium from the gut. That is, she doesn't have to work hard to get it from the gut because her needs during the dry period are minimal (30 g per day). However, this is a disadvantage at calving because her ability to actively absorb calcium from the gut is reduced. She must now actively pursue absorption of calcium from the gut, but because these mechanisms were not in use it takes a few days to reactivate them. Thus because she cannot respond quickly her blood calcium levels are depleted and milk fever develops. It is interesting to note that feeding cows very high levels of calcium may also reduce the incidence of milk fever by making it easier for the cow to absorb calcium from the gut (10).

Phosphorous. Close-up rations high in phosphorous (greater than 80 g/day) have also been associated with an increase in the incidence of milk fever. Currently levels of no greater than 40 g/day are recommended (9). High phosphorous levels will decrease the production of the active form of vitamin D which is an important player in the absorption of calcium from the intestine.

Anion-Cation Balance. Recent studies suggest that the anion-cation balance of the pre-partum diet is important in the development of milk fever. Close-up rations high in anions such as chloride and sulphur are associated with a decrease in the incidence of the disease. Diets high in cations such as sodium and potassium are associated with an increased incidence of milk fever. One analysis of several feeding trials suggests that the level of dietary sulphur and the anionic-cationic balance had the greatest influence on the development of milk fever. Increasing the sulphur concentration decreased the risk of developing milk fever. This has led to the feeding of anionic diets in the close-up dry period. These diets will increase the levels of active vitamin D thereby increasing the intestinal absorption of calcium. In addition they may aid in the calcium resorption from bone (6).

Clinical Signs

Three stages of the clinical disease have been described.

Stage 1. This is a brief stage of excitement, hypersensitivity, and muscle tremor. The animal is reluctant to move and is not interested in eating. When the animal moves the gait is unsteady and they will frequently stumble or even fall.

Stage 2. This stage is characterized by recumbency. The animal is usually sitting up, depressed, and has her head turned into the flank. The muzzle is dry, the skin and extremities are cool. The rectal temperature is usually decreased (36 to 38 degrees C), the heart rate is increased, and a mild bloat may be present.

Stage 3. At this stage the animal is very depressed almost comatose in some instances. This stage is characterized by lateral recumbency that is the cow is unable to sit up at this point. Bloat is common at this stage because of their position. If these animals are not treated promptly death will follow quickly.

Control and Prevention

When examining control and prevention of milk fever three main methods are employed. These include manipulation of the close-up ration, the administration of calcium gels, and the administration of vitamin D and its analogues. As stated previously our target is to have less than 5% of susceptible cows develop clinical milk fever.

Close-up Ration.

If possible keep calcium levels below 100 g per day. Calcium levels less than 50 g per day are reliable and effective, but difficult to achieve with our forages in western Canada.

Ensure phosphorous levels are no greater than 80 g per day. Levels currently recommended are no greater than 40 g per day.

Manipulate the anion-cation balance of the ration. This is a more practical approach for most producers feeding legume or grass hay. With many of these forages it is impossible to restrict calcium to prepartum cows because of the high levels commonly present in these feeds. In order to implement this practice it is important to have your forages analyzed for the main anions (Cl and S) and cations (Na and K) as well as calcium and phosphorous. Then the balance can be adjusted using anionic salts such as calcium chloride, magnesium sulphate, ammonium chloride, and ammonium sulphate. Often a blend of these salts is employed. Because these salts are not palatable they must be mixed with a TMR, added to silage, or mixed with 3 to 4 kg of a grain mix with a flavoring agent such as molasses. Cows must receive these diets for at least ten days before calving to receive maximum benefit (9). Close attention to dietary levels of Mg, S, Cl, and calcium, nonprotein nitrogen, and degradable protein (DIP) is important. Flow charts that aid in the formulation of these rations are available and should be followed closely(3).

Avoid overconditioning of dry cows and late lactation cows as their intake postpartum will be decreased and make them more susceptible to milk fever.

Provide a comfortable calving area such as a well bedded box stall or calving shed which affords comfort and the ability to exercise.

Calcium Gels. Calcium gels are gaining popularity in the prevention of milk fever. There are several commercially available gels, but not all have the same calcium concentrations. Good success can be achieved by giving high risk cows a tube of gel (tube should contain at least 150 g of calcium) 24 hours before, at the time of calving, and 10 to 14 hours after calving. The gels are easy to administer and quite safe. The only disadvantages they have are that they are quite bitter and they are more expensive than traditional treatments.

Vitamin D. Vitamin D3 injected intramuscularly has been used for many years to prevent milk fever. Once converted to its active form it will increase the intestinal absorption of calcium. The traditional dose of D3 has been 10 million units given 2 to 8 days before calving. A dose of 1 million units per 45 kg has given better results consistently (11). If the cow does not calve within 8 days a second dose of 10 million units is given.

There is ongoing research into the use of different forms of vitamin D. It is difficult to give good recommendations on these products at this time because we have little clinical experience with them.

References

1. Bigras-Poulin, M. 1992. Preventative Veterinary Medicine 10:79.
2. Boda, J.M. and H.H. Cole. 1956. Journal of Dairy Science 39:1027.
3. Brockman, R.P. and B. Laarveld. 1986. Livestock Production Science 14:313.
4. Dohoo, I.A. and S.W. Martin. 1984. Canadian Journal of Comparative Medicine 48:1.
5. Dohoo, I.R. 1983. Preventative Veterinary Medicine 1:321.
6. Gaynor, P.J. 1989. Journal of Dairy Science 72:2525.
7. Halse, K. and O. Magstad. 1975. Norsk. Vet.Tidsskr.87:311.
8. Markusfeld, O. 1985. Veterinary Record 116:489.
9. Oetzel, G.R. 1994. Formulation Strategies for Feeding Anionic Salts to Dry Cows. In: Seminar #18 - 27th Annual Conference of the American Association of Bovine Practitioners. Pittsburgh, Pennsylvania.
10. Oetzel, G.R. 1991. Journal of Dairy Science 74:3900.
11. Radostits, O.M., D.C. Blood, and C.C. Gay. 1994. Metabolic Diseases. In: Veterinary Medicine. Bailliere Tindall, London, pp. 1310 - 1358.
12. Weirda, A. 1985. Veterinary Record 116:284.