Transition cow metabolic problems

Proper dry cow nutrition focuses in large part on reducing the incidence of metabolic problems around calving time. Metabolic problems are caused primarily by nutrition. They usually require treatment by a veterinarian or producer. One metabolic problem often leads to others and the final result is lost milk, poor reproduction, and maybe even a lost cow.

Milk Fever

Milk fever, also known as parturient paresis, is low blood calcium. On average, 5-6% of cows will experience clinical milk fever. When the level of calcium in the blood gets too low (<5 mg/dl), nerve and muscle function is lost; the cow goes down and if untreated, can die. Milk fever is fairly easy to treat using intravenous calcium injection. Mild cases in which the cow is not down may be treated with oral calcium chloride or calcium propionate. The real problem is that milk fever predisposes cows to other health problems including ketosis, retained placenta, displaced abomasum, and mastitis. Cows experiencing milk fever release more cortisol. This inhibits the immune system promoting retained placenta, metritis and mastitis. Also, the effects of low calcium on muscle function include the muscle at the end of the teat, opening up the teat to more infection. Weak muscle contractions in the stomach can result in displaced abomasums. Finally, milk fever will reduce intake, promoting ketosis.

It has been estimated that 50% of cows have sub-clinical milk fever on calving day ( 5-7 mg/dl). These cows have no noticeable milk fever symptoms but they eat less and are more susceptible to other health problems. Many times I have been called to a farm to figure out why so many cows are having retained placentas and ketosis and found that these problems were caused by low blood calcium at calving time.

Cows need a lot of calcium to make colostrum and milk. Hormones normally work to mobilize calcium from the cow’s bones and to increase the efficiency of dietary calcium absorption at calving time. The hormones keep blood calcium at normal levels (9-10 mg/dl). Unfortunately, these hormones are inhibited when diets high in potassium or sodium are fed. These minerals are cations. They alkalinize the blood making its pH higher. High potassium will also decrease the availability of dietary magnesium. Low blood magnesium will prevent the cow’s system from recognizing low blood calcium levels; further decreasing hormone production, calcium mobilization, and calcium absorption. There are two ways to balance the diet during the last three weeks before calving to make sure that a cow maintains normal blood calcium concentrations.

Method #1 for Controlling Milk Fever --- Reduce Dietary Cations

You can feed a low potassium (<1.5%) and low sodium (<0.15%) diet. The easiest way to do this is to feed corn silage and only grasses that weren’t fertilized with manure. Analyze forages for calcium, magnesium, sodium, potassium, chloride, sulfur, and phosphorus. Balance diets for recommended mineral levels. Do not include any buffer such as sodium bicarbonate in the diet and reduce salt levels. This diet will keep the pH of the cow’s blood low, helping the cow to respond to natural hormones designed to pull calcium from the bone and intestine. This is the preferred way to control milk fever because these diets are usually palatable, helping cows to maintain better feed intake right up until calving. This method is also less expensive. The dietary magnesium level should be at least 0.25%. Some nutritionists recommend that it should be 0.40%.

Careful attention must be paid to fertilization practices and forage inventory in order to successfully control milk fever using a low potassium, low sodium diet. The goal is to keep the potassium level in forages below 2%. It is best to test soils, specifically set aside fields for dry cow grass, and control potassium application, primarily by reducing manure application. Harvest and set aside enough low potassium grass for use in the pre-fresh ration with corn silage all year long. First-cuttings usually contain more potassium than later cuttings. Watch out for pastures and bedding which cows may eat. They may be high in potassium.

Method #2 for Controlling Milk Fever --- Counteract Cations with Supplemental Anions

You can make the cow’s blood acidic by adding anionic products to the diet during the last three weeks before calving. This method must be used when no low potassium forages are available. In the past, sulfates such as ammonium sulfate, calcium sulfate (gypsum), and magnesium sulfate were used as anionic sources. Now, chlorides such as calcium chloride, magnesium chloride, and ammonium chloride are recommended over sulfates because they have been shown to be more effective. There are also commercial anionic products, for example, Bio-Chlor® and Soy-Chlor®.

To effectively use anionic products, first analyze forages for calcium, magnesium, sodium, potassium, chloride, sulfur, and phosphorus. Adjust the diet so that the dietary cation-anion difference (DCAD) is –5 to –10 mEq/100 g (-23 to –45 mEq/lb). DCAD is calculated as [(Potassium (K) + Sodium (Na) – (Chloride (Cl) + Sulfur (S))]. Most diets will need 0.6 to 0.8% chloride to significantly decrease DCAD. When using anionic products, maintain diet calcium at 1-1.5%. Dietary magnesium should be at 0.40%, phosphorus at 0.35%, and sulfur at 0.45%.

Anionic products are expensive and unpalatable. They should only be used if dietary potassium cannot be sufficiently reduced. Monitor dry matter intake. Pre-fresh cows should average at least 23 pounds of dry matter intake per day. Low intakes during the pre-fresh period can cause fresh cow problems.

The goal when lowering DCAD is to make the cow’s blood more acidic. Urine pH can be used to monitor blood pH. Average urine pH the last week before calving should be between 6.0 and 6.5 for Holsteins and for Jerseys, 5.8 to 6.2. If the average urine pH falls below 5.5, the cow’s blood is too acidic and dry matter intake will be down. It is best to measure urine pH about 4 to 6 hours after feeding. Increase or decrease dietary chloride according to the urine pH.

The Old Milk Fever Theory

In the past, it was believed that diets high in calcium caused milk fever. It is now recognized that the apparent successes of these diets were due to a reduction of dietary potassium at the same time as calcium was reduced. For example, alfalfa usually contains high levels of both potassium and calcium so both will be reduced when alfalfa is replaced with grass or corn silage. Reducing dietary calcium to less than 15 grams per day will reduce milk fever but it is almost impossible to get a diet that low.

Retained Placenta and Metritis

On average, 8-10% of dairy cows won’t get rid of all or part of the placenta by 24 hours after calving. Retained placentas, also known as retained fetal membrane (RFM), delay uterine involution and increase the incidence of metritis. Metritis is a uterine infection.

In a healthy cow, the immune system attacks specific cells to release the placenta after calving. Hormonal changes and the outpouring of antibodies in colostrum naturally compromise the cow’s immune system at calving time. By enhancing the immune system through nutrition, the incidence of retained placenta and metritiscan be reduced. Selenium (0.3 ppm) and Vitamin E (1000 IU/day) help to prevent membrane damage. Some nutritionists recommend a higher level of Vitamin E (2000 IU/day) two weeks before and after calving. Providing enough energy for the immune system is also important, especially during the last 3 weeks before calving (0.70 Mcal NEl/lb). If you know a cow is carrying twins, put her on a prefresh diet 5-6 weeks before calving. Ensure that trace mineral levels are adequate and that no particular minerals, like iron, are fed in excess such that they reduce the absorption of others. Copper (15 ppm) and zinc (60 ppm) supplementation in the sulfate form or organic form is recommended. Avoid stress. If a cow is stressed, she will produce cortisol, a potent inhibitor of the immune system. Cows are stressed if they aren’t comfortable and if they have health problems.

Maintain body muscle stores with protein (12-13% CP for the far-out dry cow and 14-15% CP for the last 3 weeks before calving) and maintain muscle function. Cows need muscle for uterine contractions. One study from Cornell indicated that feeding higher levels of protein during the dry period decreased the incidence of retained placenta. Cows with milk fever have reduced muscle contractions.

Fat cows (>3.75 BCS) are more likely to have a retained placenta. This may be because they don’t eat as well as thinner cows do during the last week before calving. It may also be because fat cows have more problems calving and that is associated with retained placenta. Cows who have had twins are also more likely to have retained placenta. Heifers that are not adequate size (< 1350 pounds) at first-calving are also more likely to have retained placenta, especially if a calving ease sire was not used. When calving is induced with drugs, expect retained placenta.

Displaced Abomasums

Displaced abomasums can be either left-sided or right-sided. The most common is the left-sided (LDA) where the abomasum moves from its normal spot on the right side of the abdomen floor to the left. Often it occurs when cows consume diets high in grain and low in effective fiber. It can also be caused simply by inadequate dry matter intake. Rumen fill and stomach motility are reduced, the abomasum becomes filled with gas and partially digested feed, and then the abomasum moves. Usually LDA occurs within a week after calving but it can occur in cows in the later stages of lactation if their diet is drastically changed or effective fiber is minimal. Surgery is usually necessary to treat LDA but sometimes rolling the cow or blindly suturing can remedy the situation.

Maintaining intake, especially long, effective fiber intake, can prevent LDA. It is also helpful to make ration changes slowly and bring cows up on grain gradually (one pound per day) after calving. Milk fever, retained placentas, and ketosis must also be controlled. Milk fever will decrease intake and reduce the muscle activity of the gastrointestinal tract. Retained placentas and ketosis will reduce intake.

Right-side displacement (RDA) is more rare. It is caused by the same factors that cause LDA. But, RDA results in death more often than LDA. With RDA, the abomasum twists and this results in a blockage of flow of partially digested feed through the abomasum. It must be treated by surgery right away.

Ketosis (Acetonemia)

Ketosis is the incomplete use of body fat by the cow. When the cow's energy demands for milk production exceed her energy supply, she begins to use body fat as an energy source. Fats are first broken down into smaller pieces, called non-esterified fatty acids (NEFA's), and carried to the liver. At the liver, NEFA’s are broken down to form acetate. Through this process, energy is generated. Acetate must then be broken down to carbon dioxide and water to yield more energy, however, this process requires some propionate. If there is not enough propionate available, the excess acetate builds up in the liver then acetate molecules combine to make acetone, acetoacetate, and beta-hydroxybutyrate. These ketones are released from the liver into the cow's bloodstream, causing the ketosis symptoms.

A clinically ketotic cow will not produce much milk, will not eat much (especially grain), and will lose body weight rapidly. Some management experts believe that reduced brain glucose during ketosis reduces the ability of cows to deal with new situations such as headlocks at the feed bunk and automatic waterers. As ketosis becomes more extreme, the cow may be nervous and have a sweet, acetone smell to her breath. Fatter cows (BCS>3.75) are more prone to ketosis.

Higher dry matter intake will increase propionate production. That makes fresh, adequate feed (24 hrs/day) absolutely critical for pre-fresh and fresh cows. Cows make propionate in their rumens primarily from starches and sugars provided from feeds like corn and molasses. For this reason, it is generally recommended that pre-fresh diets contain 32-33% NFC. Cows can also be fed propionate directly in the form of calcium propionate (0.25 pound/day) or commercial propionate supplements. There is Cornell research in which the protein content of the first-calf heifer diets was boosted from 12 to 15% using bypass protein. Those with the extra protein maintained body condition better.

Fatty Liver

Fatty liver syndrome is the accumulation of fat within the cow's liver. Excessive fat stores in the liver do not occur while the cow is putting fat on her back. Instead, fatty liver is the result of a cow mobilizing body fat and then collecting some of that fat in the liver. Thus, the liver becomes fat while the cow is losing weight. Fatty liver syndrome (> 20% fat) impairs the function of the liver, increases disease incidence, reduces fertility, and sometimes leads to death. Once deposited in the liver, fat levels are not reduced until the cow achieves a state of positive energy balance about 5 to 10 weeks after calving. As with ketosis, fatter cows (BCS > 3.75) are more likely than thinner cows to experience fatty liver syndrome during early lactation. Like ketosis, negative energy balance is the primary cause of fatty liver. Stress can also cause fatty liver. When a cow is stressed at calving time, her hormones trigger a rise in blood fat concentrations. Poor environmental and/or handling conditions can stress the cow.

Udder Edema

Udder edema is the accumulation of fluid in the udder and sometimes also in the cow’s belly. Some edema is normal around calving time. But, excessive edema will make milking more difficult and can do permanent damage by breaking down udder supports. Incomplete removal of milk at milking time may result in lower milk yield for the lactation. Udder edema results from increased blood flow to the udder accompanied by decreased blood flow from the udder. Increased permeability of the blood vessels allows fluids to leak out and accumulate.

The reasons for udder edema aren’t entirely certain. It is more prevalent in first-calf heifers, possibly because they have less vascular development. The tendency of some cows to get udder edema may be inherited. Udder edema has been related to feeding high amounts of energy, sodium, or potassium. Generally, it is recommended that sodium (Na) stay below 0.15% of the diet and potassium (K) below 1.4% of the diet during the last three weeks before calving to avoid udder edema.

University of Tennessee researchers suggest that "oxidative stress" may be a cause of udder edema. Even though oxygen is essential for life, the cow needs to metabolize it and get rid of it otherwise it can be toxic. When metabolism increases, such as for milk production, more free oxygen may end up in the udder. Oxygen reacts with mycotoxins in the feed, products from heat-damaged feed, and excessive iron and molybdenum. These are all called pro-oxidants. Products from these chemical reactions damage cell membranes, causing udder edema. The reactivity of iron is more likely during times of stress, like at calving. Zinc, copper, manganese, magnesium, Vitamin E, and selenium all help to reduce these oxidative reactions. These nutrients are either called anti-oxidants or are needed to make anti-oxidants. Adequate protein is also important. The goal is to provide enough anti-oxidants to adequately defend against pro-oxidants. University of Tennessee researchers recommend that the pre-fresh and post-fresh diet contain 0.3 ppm selenium (the legal limit), 20 ppm copper, 60 ppm each of zinc and manganese, and 0.25% magnesium, plus 1000 ppm Vitamin E. Oxidative stress is likely also a factor promoting retained placenta and mastitis.

Grass (Magnesium) Tetany

Grass tetany is low blood magnesium. Advanced symptoms look like milk fever. Early symptoms include excitement and twitching of muscles. Cows may also grind their teeth, convulse, and salivate a lot. Grass tetany is controlled with adequate dietary magnesium. The minimum dietary recommendation is 0.25% magnesium but some nutritionists recommend 0.40%. Other than at calving time, magnesium tetany is also seen when cows graze lush, grass pasture and dietary magnesium absorption is low.

Summary

 

Metabolic problems are linked to nutrition. One metabolic problem often leads to others. Milk fever is low blood calcium. The incidence of milk fever can be controlled by reducing dietary cations or by counteracting dietary cations with supplemental anions.
Retained placenta is failure to get rid of the placenta by 24 hours after calving. Maintaining the immune system and body muscle stores can prevent retained placenta. Fatter cows and twinning cows are more likely to have retained placenta.
Displaced abomasums are controlled with adequate dry matter and fiber intake.
Ketosis and fatty liver are reduced with adequate propionate supply.
Propionate increases with dry matter intake and concentrate intake. Fresh, adequate feed and forage should be supplied to transition cows. Propionate additives are available.
Udder edema is the accumulation of fluid in the udder. It is related to feeding high amounts of energy, sodium, or potassium. It may also be caused by oxidative stress.
Grass (magnesium) tetany is low blood magnesium. It is controlled with adequate dietary magnesium. 

 

  • Metabolic problems are linked to nutrition. One metabolic problem often leads to others.
  • Milk fever is low blood calcium. The incidence of milk fever can be controlled by reducing dietary cations or by counteracting dietary cations with supplemental anions.
  • Retained placenta is failure to get rid of the placenta by 24 hours after calving. Maintaining the immune system and body muscle stores can prevent retained placenta. Fatter cows and twinning cows are more likely to have retained placenta.
  • Displaced abomasums are controlled with adequate dry matter and fiber intake.
  • Ketosis and fatty liver are reduced with adequate propionate supply. Propionate increases with dry matter intake and concentrate intake. Fresh, adequate feed and forage should be supplied to transition cows. Propionate additives are available.
  • Udder edema is the accumulation of fluid in the udder. It is related to feeding high amounts of energy, sodium, or potassium. It may also be caused by oxidative stress.
  • Grass (magnesium) tetany is low blood magnesium. It is controlled with adequate dietary magnesium. 

References:

Chandler, P. 1999. Transition cow feeding and management methods studied. Feedstuffs. December 13, 1999, p. 10.

Curtis, C.R., H.N. Erb, C.J. Sniffen, R.D. Smith, and D.S. Kronfeld. 1985. Path analysis of dry period nutrition, postpartum metabolic and reproductive disorders, and mastitis in Holstein cows. J. Dairy Sci. 68:2347.

Davidson, J., L. Rodriguez, T. Pilbeam, and D. Beede. 1995. Troubleshooting prefresh rations with anionic salts. Hoard’s Dairyman. November 1995, p. 741.

Goff, J. 1999. What you can do to prevent retained placenta. Hoard’s Dairyman. September 25, 1999, p. 660.

Goff, J.P. and R.L. Horst. 1996. To understand milk fever is to prevent it. Hoard’s Dairyman, October 25, 1996, p. 722.

Goff, J.P. and R.L. Horst. 1997. Steps you can take to avoid milk fever. Hoard’s Dairyman. January 10, 1997, p. 12.

Grummer, R. 1993. Feed to avoid fatty liver and ketosis. Hoard’s Dairyman. October, 1993, p. 754.

Hutjens, M.F. 1991. Dry cow care can boost milk 1,000 to 2,000 pounds. Hoard’s Dairyman. September 25, 1991, p. 702.

Mueller, F.J., J.K. Miller, M.H. Campbell, and F.C. Madsen. 1998. Prevention of udder edema in dairy cows. In: Proceedings of the Tri-State Dairy Nutrition Conference, Fort Wayne, IN, April 21-22, 1998, p. 79.

Oetzel, G.R. 1994. Calcium chloride gels help prevent milk fever. Hoard’s Dairyman. June 1994, p. 443.

Oetzel, G.R., J.P. Goff, and R.L. Horst. 1999. How to prevent low blood calcium and milk fever. Hoard’s Dairyman. February 25, 1999, p. 162.

Osborne, J. Ketosis.

Shearer, J.K. and H.H. Van Horn. 1992. Metabolic diseases of dairy cattle. In: Large Dairy Herd Management, Edited by H.H. Van Horn and C.J. Wilcox, American Dairy Science Association.

Van Saun, R.J., S.C. Idleman, and C.J. Sniffen. 1993. Effect of undegradable protein amount fed prepartum on postpartum production in first lactation Holstein cows. J. Dairy Sci. 76:236.

Related Links:

Managing Dairy Cows to Avoid Abomasal Displacement
Rick Grant, Ph.D.

Dairy Cow Health and Metabolic Disease Relative to Nutritional Factors
Duane Rice and Rick Grant, University of Nebraska - Lincoln

Therapeutic Nutrition for Dairy Cattle
V. Ishler, M. O’Connor, and L. Hutchinson, Penn State University

A Successful Transitioning Program
Purina Mills
Click on "Programs" Tab, then click on "Transition Cow" tab

Dairy Cow Diseases and Disorders, In: Feeding the Dairy Herd, North Central Regional Extension Publication
J.G. Linn et al.

Author

Mary Beth de Ondarza

Mary Beth de Ondarza
45 articles

Nutritional consultant for the dairy feed industry at Paradox Nutrition, LLC.

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Dr. de Ondarza received her Ph. D. from Michigan State University and her Masters Degree from Cornell University, both in the field of Dairy Nutrition.

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Paradox Nutrition

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Paradox Nutrition, LLC is a nutritional consultation business for the dairy feed industry. Mary Beth de Ondarza, Ph.D. is the sole proprietor.

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