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Chapter 18 Feeding dairy.

... all the really good ideas I'd ever had came to me while I was milking a cow.

G. WOOD

The nutritional phases in the dairy production cycle, illustrated in Figure 18-1, include:

Cows: Fresh, mid-lactation, late lactation, early-mid dry, close-up dry Calves and heifers: Liquid feeding/calf starter, calf starter, prebred heifer, postbred heifer

A sample growth rate is plotted in Figure 18-2.

COWS

Fresh Cows

Fresh cows are cows that have recently transitioned from pregnancy through the process of parturition and on to lactation. The health and productivity of the fresh cow is dependent on the success of this transition. The period of time from the last 3 weeks of the dry period to the first 3 weeks of lactation is described as the transition or periparturient period. Transition cows are cows that are changing from the hormonal and metabolic status characteristic of the non-lactating (dry) cow to the hormonal and metabolic status of the lactating cow. There are many problems that may occur if the transition proceeds poorly. These include:

Ketosis

Fatty liver syndrome

Displaced abomasum

Retained placenta

Mastitis

Metritis

Milk fever

Acidosis

[FIGURE 18-1 OMITTED]

[FIGURE 18-2 OMITTED]

The primary nutritional consideration during the transition period is meeting the cow's energy requirement. This is because the cow's need for energy is increasing at a time when her appetite is declining (Figure 18-3). Normally, cow dry matter intake (DMI) falls by approximately 30 percent during the transition period (Hayirli, Grummer, Nordheim, & Crump, 2002). With the exception of milk fever and acidosis, the energy deficit of the transition cow is a contributing factor to all of the problems that may be experienced by the transition cow.

Recall from the discussion of additives in Chapter 3 that ionophores are products that increase the efficiency with which ruminants are able to use feed energy to meet their maintenance energy needs. These products may, therefore, be useful in transition cow diets to help minimize the energy deficit and alleviate all the problems associated with it. However, most studies have shown that use of ionophores results in reduced dairy matter intake, and this would deepen the energy deficit. One ionophore has recently been approved for use in dry and lactating dairy cows in the United States. The choice of whether to use an ionophore in transition cows and lactating cows will depend on whether the improvement in energy efficiency more than offsets the reduction in DMI. Transition cow problems are discussed later in this chapter under "Dairy Feeding and Nutrition Issues."

[FIGURE 18-3 OMITTED]

Dairy cattle, like beef cattle, are usually managed to maintain a 12-month calving interval. To do this, cows must become pregnant (settle) within about 80 days of calving. This is because the gestation length is about 282 days. If cows are open much more than 80 days, it will take more than 365 days to complete the reproductive cycle. The period of 80 days postcalving corresponds to the period of time when the cow is peaking in milk production and continues to run an energy deficit. Following calving, the cow's ovaries remain inactive (ovulation does not occur) until energy balance progresses beyond its most negative value (the nadir) and is returning toward balance. Specifically, the cow's first postpartum ovulation occurs 1 to 2 weeks after the negative energy balance nadir is reached (Canfield & Butler, 1991).

The most important factor determining the productivity and profitability of fresh cows is DMI. Feeding and management decisions that lead to increased DMI by cows in early lactation will always result in increased profits. DMI is limited by the resident time of feed in the digestive tract. DMI, then, is potentially increased as the rate of feed removal from the rumen increases. Feed material is removed from the rumen by one of four means:

1. Feed may be colonized and fermented by rumen microbes, which incorporate feed nutrients into microbial cells. These cells are regularly washed out of the rumen.

2. Microbial activity may process a portion of the feed into gases, which are eructated.

3. Microbial activity may turn feed material into valuable compounds that are absorbed through the rumen wall.

4. Finally, feed material may be reduced in size to small and dense particles that pass out of the reticulum and rumen into the omasum.
Figure 18-4

Predicting rumen pH using
peNDF

Rumen pH = 5.425 + (0.04229 x peNDF), where penNDF is expressed as a
percentage of ration dry matter.
Example: Given peNDF in ration dry matter of 20%.
5.425 + (0.04229 x 20) = 5.425 + 0.846
                       = 6.27, predicted rumen pH


Diets composed of high levels of coarse forage are processed slowly and accumulate in the rumen. At some point, the gut is full and eating stops. As coarse forage is replaced by grain in these diets, the rate of feed removal increases because grain is removed more rapidly from the rumen than is forage. This allows for increased DMI. However, as forage is replaced by grain, a decreased amount of saliva is produced because less chewing is required. Saliva is the primary source of buffer for the rumen microbes. At the same time, increasing amounts of acid are being produced as the microbes ferment the grain. As forage continues to be replaced by grain, the rumen pH will begin to fall. In the CNCPS v.5 (Fox, Tylutki, Tedeschi, Van Amburgh, Chase, Pell, & Overton., 2004) and in the companion application to this text, the rumen pH is predicted from the amount of physically effective neutral detergent fiber (peNDF) in the ration (Figure 18-4).

The rumen bacteria that are most sensitive to decreases in pH are those that work on the forages. When these microbes begin to suffer, DMI will decline because forages are not being removed from the rumen as rapidly. Further decreases in rumen pH may result in systemic acidosis, which is a threat to the well-being of the cow. Acidosis is discussed in Chapter 20.

Mid-Lactation and Late Lactation

Lactating cows should be fed a ration that matches their production potential. In general, a nutrient deficiency during lactation will result in reduced milk production rather than a reduced level of that nutrient in the milk produced. Both deficiencies and excesses will have a negative impact on farm profitability. Meeting the nutritional requirements for lactating cows as they progress through their lactation is achieved by establishing groups on the farm, developing rations for those groups, and moving animals into the appropriate group at the proper time.

A simplified daily time budget for lactating dairy cattle (Grant, 2003) would include 9 to 14 meals eaten during 3 to 5 hours per day. This budget would also include 10 to 12 hours lying down and resting, 7 to 10 hours ruminating, 30 minutes drinking, and 2 to 3 hours in the milking parlor. It has been suggested that for each hour additional rest beyond 7 hours and up to 14 hours, cows may be expected to produce 2 lb. additional milk daily (Albright, 2001). Studying the time budgets of lactating dairy cows shows how animal management can trump animal nutrition when it comes to animal performance.

Energetic efficiency would be greatest if cow body condition did not cycle; that is, if the requirement for energy was always matched by the intake of feed energy. However, during early lactation, the high-producing cow will be in an energy-deficit situation. To maintain high levels of milk production, the cow will need to draw on stored reserves of body fat as a secondary source of energy. During lactation, cow body condition will change as she uses these energy reserves and loses weight during the first 70 days or so, then replenishes these reserves and gains weight as milk production declines. As with beef cattle, a body condition scoring system is used with dairy cattle to assess body fat reserves and overall energy status. The dairy system uses scores of 1 to 5 as described in the following chapter in Table 19-2.

Ideally, feeding management is such that weight loss during lactation corresponds to no more than one body condition score (BCS). Given that the target body condition score for the fresh cow is 3.5 to 4.0, most cows should not fall below a BCS of 2.5 during their lactation. Late lactation is the best time to make feeding adjustments to increase or decrease cow body condition in preparation for the next lactation.

Early-Mid Dry and Close-Up Dry

Metabolic and nutritional disorders such as ketosis, milk fever, retained placenta, and displaced abomasum (DA) all have their root cause in the nutritional management during the months leading up to calving (the dry cow period). In the dairy industry, there is currently a great deal of interest in the possibility of reducing the dry period from the traditional 60-day duration and even eliminating it altogether (Annen, Collier, McGuire, & Vicini, 2004). Although more research is needed to consider the biological processes that occur within the mammary gland during the dry period (Bachman & Schairer, 2003), there is a paucity of research on what effect a shortened dry period would have on the incidence of metabolic disorders (Grummer & Rastani, 2004). It is likely that with proper management, a shortened dry period will not necessarily be associated with increased incidence of metabolic disorders.

A successful dry cow feeding program consists of the following.

1. Providing proper nutrition for the development of the fetus. About two thirds of the weight of the newborn calf is gained during the last 2 months of gestation. The fetus of a calf weighing 90 lb. at birth would, therefore, increase in weight about a pound a day during a 60-day dry period. Ashortage of nutrients at this time will result in the birth of weak or dead calves.

2. Preparing the digestive system for the upcoming lactation. The stress of feed change can be minimized by preparing the cow during the last portion of the dry period. This involves the introduction of grain to the diet to develop the proper microbial population. During the 2 weeks prior to freshening, dry cows and heifers should be fed increasing amounts of grain up to a maximum of 0.5 percent of the body weight (NRC, 1989). It is inadvisable to use the lactation ration as part of the dry cow diet, even for only the last few weeks of the dry period. This is primarily due to the fact that the mineral and vitamin needs of lactating cows are dramatically different from those of dry cows. In addition, lactation rations often contain buffers to combat the acids generated from the high-grain diets they are fed. Dry cows will not have the high-grain diet and so will not have high acid production. As a result, dry cows fed buffers may have undesirably high rumen pH values. Some minerals, particularly magnesium, are absorbed with decreasing efficiency as rumen pH increases. Magnesium deficiency has been implicated in some postcalving disorders.

3. Retooling the cow's metabolism for the challenges of lactation. Many metabolic pathways must be established and redirected to support lactation. Included are pathways that involve the generation of glucose needed for milk lactose synthesis, the mobilization of body fat stores for milk fat synthesis, and the management of body mineral stores to ensure that the cow's health is maintained, even as large amounts of mineral leave the body in milk.

4. Maintaining the proper body condition. In most situations, the focus of dry-cow feeding is not so much rebuilding body stores as it is avoiding overconditioning. Management of the cow's body weight is an important goal because cows that are dried off fat are more likely to have difficulties at the end of their dry period when they calve. Ideally, cows are dried off at the same BCS as that at which they will calve, and there is no weight change during the dry period. The recommended BCS for cows at calving is 3.5-4.0 (Table 19-2). To achieve the 3.5-4.0 BCS in the cow at dry-off time means careful management of her feeding program, and has implications on grouping strategies used at the farm.

CALVES AND HEIFERS

The objective of the calf-raising program is to keep the calf alive, healthy, and growing at a rate at which she will be large enough to breed by 14 months of age.

Liquid Feeding/Calf Starter

The structure of the cow's placenta is described as epitheliolchorial. This type of placenta does not allow antibody immunoglobulins to pass from the cow into the blood of the fetal calf. These antibody immunoglobulins are acquired by the neonatal calf through colostrum. Colostrum, or first milk, is secreted by the cow the first few days following calving. As is the case with other mammalian livestock, colostrum should be consumed by the neonatal calf as soon as possible. If calves are left with the dam to suckle, many will not receive adequate colostrum, so colostrum consumption should be a closely managed activity. An esophageal feeder may be used to get colostrum into calves if they will not drink by themselves. It is possible to store excess high-quality colostrum from older cows by freezing. Before use, frozen colostrum should be thawed in warm water. The importance of colostrum to the neonatal calf cannot be overestimated. Colostrum is discussed in Chapter 20.

The recommendations for colostrum consumption for all ruminants are that (1) neonates should receive an amount of colostrum that is equivalent to 10 percent of the birth weight or 1.5 ounces per pound of body weight within 12 hours of birth, and that (2) half this amount should be ingested within 2 hours of birth, the sooner the better. For an 80-lb. calf, this amounts to about 1 gallon (4 quarts) of high-quality colostrum within the first 12 hours of birth and at least 2 quarts of colostrum within 2 hours of birth. Colostrum should be fed for the first 3 days of life at a rate of 4 quarts per day.

When the calf is 4 and 5 days of age, milk or milk replacer should be fed at a rate of 1 quart twice daily. On day 6 through weaning, calves should be fed 5 percent of body weight twice daily for a maximum of 10 percent per day (milk and milk replacer weigh about 8 pounds per gallon). All milk-feeding equipment should be kept clean and sanitized.

Milk replacers are intended to replace whole milk as calf feed. The reason for feeding milk replacer is an economic one: the cost of the milk replacer is less than the value of whole milk.

Feed mills have available several types of milk replacers. The most expensive contain protein from skim milk, casein, and whey. The least expensive generally contain untreated soybean protein. There are also milk replacers available that are soybean based but have been treated to improve the feeding value for calves. Unlike milk replacers made from milk protein sources, those made from untreated soybean protein contain enzyme inhibitors, and for some calves, allergens. The enzyme inhibitors will reduce protein digestion and retard growth in calves. Another concern with soybean-based milk replacers is the amino-acid balance. Compared to milk protein, soybean protein is somewhat deficient in methionine and, therefore, soybean-based milk replacers are often fortified with this amino acid. Antibiotics are also sometimes added to milk replacers to aid in growth promotion and prevention of bacterial scours.

When the calf is 4 days old, a calf starter should be offered fresh daily along with clean, fresh water. A high-quality calf starter should be highly palatable and nutritionally balanced. Feedstuffs often included in calf starters include cracked or flaked corn, oats and oat products, beet pulp, molasses, soybean meal, and milk products. Although the functional rumen is renowned for its ability to ferment forage, it is the volatile fatty acids from the digestion of the grain in calf starters that stimulate early rumen development.

The following guidelines will help determine when to wean the calf.

1. The calf should be at least 4 weeks old.

2. The calf should be eating 1.5 to 2 lb. daily of calf starter.

3. The above rate of calf starter consumption should have occurred for 3 consecutive days.

4. The size and health of the calf should be considered.

On most farms, calves will be weaned at 4 to 8 weeks of age.

Calf Starter

By 8 weeks of age or about 2 weeks after weaning, calves should be eating 6 to 8 lb. of calf starter. The calf now has a functional rumen and is capable of rumination. At this time, high-quality forages should be introduced to the calf's diet. Calf starters generally contain an ionophore. Ionophores help control the protozoan disease coccidiosis. Use of an ionophore in dairy calves and heifers also consistently improves feed efficiency (Chapter 3).

Prebred Heifer and Postbred Heifer

The objective of a heifer program is to produce a well-grown heifer ready to breed early, calve early, and begin to contribute profits at an early age.

Within 2 weeks following weaning, calves should be consuming 6 to 8 lb. of starter grain. At this time, herd replacement calves should be changed to a heifer feeding program that will include forages. The heifer feeding program should include a ration balanced for all nutrients to support proper heifer growth and development.

Top-quality hay is always desirable for young heifers. If poor hay must be utilized in a dairy operation, it is best fed to dry cows or to heifers more than 1 year old. In addition to hay, hay crop silage, corn or sorghum silage, and pasture can all be useful in building balanced heifer rations. It is always important to know the nutrient content of the forages, whether of good or poor quality, so that proper supplementation can be applied to the ration(s) of which they are a part.

To the extent possible, heifers should be grouped according to nutritional need. Also, the grouping strategy used should minimize the effect of dominance hierarchies on animal access to feed. In growing heifers, both nutritional need and position in the dominance hierarchy correspond well to animal size. In practice, then, animals are grouped according to body size.

Two weeks prior to calving, the heifer should be treated and fed differently, and a separate prefresh group is desirable. At this time, the feeding strategy is designed not only to meet nutritional requirements, but also to prepare the microbes of the rumen for the high-grain diet of the lactating group(s). During the 2 weeks prior to freshening, animals should be fed increasing amounts of grain up to a maximum of 0.5 percent of the body weight (NRC, 1989). Unless the animal has an additional need for nutrients, grain beyond this level provides no additional benefit and may result in undesirable fat deposition.

The period during the 3 weeks prior to freshening to about 3 weeks after freshening is called the transition period. More is said about this critical period in the section on "Fresh Cows" and in the section on "Dairy Feeding and Nutrition Issues."

Lactating heifers have different nutrient requirements than mature cows because they are growing in addition to producing milk. Also, heifers are generally of lower rank in the herd and are less aggressive. Ideally, lactating heifers are fed separately from the cows.

DAIRY FEEDING AND NUTRITION ISSUES

Transition Cow Problems

Energy and ketosis (or acetonemia) and fatty liver syndrome

Most animals evolved in an energy-scarce environment. The milk made by mammals is, therefore, rich in energy to help ensure newborn survival. Cows acquire the energy to make this high-energy product from two sources: the energy contained in ingested nutrients from the diet and stored body fat. The energetic efficiency is higher when milk is produced using feed energy rather than the energy in stored fat, and this is one reason that high-producing cows should be managed to maximize DMI. Another reason is that when cows depend excessively on body fat to meet their energy requirement, they become ketotic.

Body fat is a good source of energy for the transition cow, but it is not a versatile source. Body fat is effectively used to make milk fat, but it is poorly used to meet the cow's other energy needs. This is important because although a significant portion of the energy cost of making milk comes from fat production (NRC, 2001), there are other energy costs involved in milk production, and these other energy costs are met with glucose, not mobilized body fat.

Where does the cow get the glucose it needs to meet the portion of its energy requirement that cannot be met by fat? The carbohydrate in feed material is a source of glucose for nonruminants. For these animals, carbohydrate is digested to monosaccharides, including glucose, which are absorbed into the blood. However, carbohydrate in the ruminant goes into the rumen, where it is used as an energy source by the microbes. Glucose of dietary origin typically makes little net contribution to the glucose supply of ruminants (Reynolds, Harman, & Cecava, 1994) because little carbohydrate passes out of the rumen.

Most of the glucose needed by the ruminant animal must be manufactured by the animal during gluconeogenesis [gluco (glucose), neo (new), genesis (creation)]. Gluconeogenesis is carried out primarily by the liver. A representation of the cow's sources and uses for glucose is found in Figure 18-5. Because glucose is used to make lactose (milk sugar) and because lactose content in milk is relatively constant (NRC, 2001), a deficiency of lactose will result in a reduction in milk production. Glucose is made from substances called glucogenic precursors. Glucogenic precursors include:

* Fermentation products (mostly propionate).

* Feed amino acids.

* Muscle amino acids.

Note that the first two sources of glucose come from the digestive tract. However, during the transition period, the cow's appetite is usually depressed, so transition cows are usually glucose deficient to some degree. A glucose deficiency is essentially the same as an energy deficiency. The energy deficiency of transition cows is probably a contributing factor to all of the transition cow problems except milk fever and acidosis.

Cows in an energy deficit are mobilizing body fat to help meet the body's energy needs. As evidence of this fact, samples of blood from transition cows in energy deficit show high levels of circulating nonesterified fatty acids (NEFA). In order to use body fat as an energy source, lipolysis must occur during which the ester bonds of triacylglycerols in fat tissue are broken. This releases glycerol and NEFA into the blood in the proportion of 1:3. Most of the fat's energy resides in the NEFA. NEFAmay be used directly by the mammary gland to make milk fat.

[FIGURE 18-5 OMITTED]

The liver takes up NEFAin proportion to its level in the blood. This is a factor in fatty liver syndrome because imported NEFA are reesterified back into triglycerides in the liver. The triglycerides remain in the liver until they can be oxidized in liver cell mitochondria or repackaged for export. Because the export process is slow relative to the import of NEFA, triglyceride may accumulate in the liver, leading to fatty liver syndrome. Symptoms of fatty liver syndrome are due to impaired liver function. Because of the wide variety of activities carried out by the liver, symptoms are nonspecific and include general weakness, poor health, reduced production, and depression.

Oxidation of liver triglyceride involves degrading triglyceride back to NEFA and sending the NEFA to the tricarboxylic acid (TCA) cycle in cell mitochondria. However, in order for NEFAto be completely oxidized in the TCA cycle, glucogenic precursors (most amino acids, propionate, and glycerol from lipolysis) must be available.

If glucogenic precursors are in short supply, as will be the case in an animal with a poor appetite, the NEFA will be incompletely oxidized. The incomplete oxidation of NEFA by the liver produces ketones (also called ketone bodies), energy-containing compounds that may be used by a few tissues of the body. Most tissues cannot use ketones, however, and their presence in the blood further depresses appetite. Because ketones are removed from the body via the lungs, they may be detected on the breath of the ketotic animal as the sweetish smell of acetone. Because ketones are also excreted via the kidneys, this same sweetish smell may be detected in urine. Other symptoms of ketosis include dullness, depression, incoordination, rapid weight loss, and a drop in milk production.

Numerous feed products have been developed to help prevent ketosis in transition cows. Table 18-1 lists and describes some of these products.

During the transition period in dairy cows, feeders must carefully manage the supply of glucogenic precursors available to the cow. The most cost-effective supply of glucogenic precursors will be propionate from carbohydrate (both NFC and NDF) fermentation in the rumen. Proteins also supply glucogenic amino acids. Maintaining a good appetite, therefore, should always be the first strategy to prevent transition cow problems.

The energy deficit that occurs at freshening is responsible not only for ketosis, but also for most of the other problems that occur during the transition period in dairy cows.

Energy and Displaced Abomasum

The displaced abomasum (DA) is strongly and consistently associated with energy nutrition. Although the nature of the link is not well understood, minimizing the energy deficit for the transition cow is the best strategy to prevent DA.

Energy and Mastitis, Metritis, and Retained Placenta

A significant component of dietary energy and protein is used to replenish the supply of the cow's white blood cells, specifically, the neutrophils. An 1,800-lb. cow has approximately 1.4 x [10.sup.11] neutrophils in its blood (Kehrli, 2001). In the cow, half this number must be replaced every 6 hours and this replacement requires a significant amount of energy. Transition cows in energy deficit, therefore, experience immunosuppression. Given the fact that the energy demand of lactation is largely responsible for the energy deficit, it is not surprising that mastectomized cows showed a much shorter period of immunosuppression following calving than did intact lactating cows (Kimura, Goff, Kehrli, Harp, & Nonnecke, 1997). Immunosuppression predisposes cows to infections such as mastitis and metritis, and it may contribute to retained placentas (Goff & Horst, 1997) due to diminished attack by neutrophils on placental tissues following parturition.

Excess Protein

Dietary protein that is degraded in the rumen becomes ammonia. This ammonia is utilized by the rumen microbes as a source of nitrogen with which to build microbial cell proteins. If a ruminant animal is fed more degradable protein than can be incorporated into cell protein, the ammonia will accumulate and may be absorbed into the blood through the rumen wall. This absorbed ammonia is converted to urea by the liver.

[FIGURE 18-6 OMITTED]

Dietary protein that passes through the rumen undegraded arrives at the small intestine. If it is digestible, most of the component amino acids will be absorbed (Chapter 7). If the animal cannot use the absorbed amino acids to make body proteins, either because the level of protein in the diet is excessive or because the quality of the protein is poor, the nitrogen is removed from the excess amino acids and it, too, is processed into urea.

Much of the blood urea is filtered out by the kidneys and excreted. A small amount of the urea in the blood is recycled in saliva. Some will exit the body in milk. Excess dietary protein may be assessed by examining blood and milk urea nitrogen levels (BUN and MUN). Protein excesses are indicated by BUN or MUN levels above 19 mg/dl. (Butler, 1998).

Excess dietary protein has been associated with reproductive problems (McCormick, French, Brown, Cuomo, Chapa, Fernandez, Beatty, & Blouini, 1999; Butler, 1998; Elrod & Butler, 1993; Canfield, Sniffen, & Butler, 1990; Bruckental, Dori, Kaim, Lehrer, & Folman, 1989; Jordan, Chapman, Holtan, & Swanson, 1983; Jordan & Swanson, 1979). The relationship between blood urea levels and reproductive performance is complex. Figure 18-6 summarizes relevant theories.

The manufacture of urea from excess dietary protein requires energy. The companion application to this text calculates the metabolizable energy that will be needed to process any excess protein into urea. This amount of energy is referred to as the urea cost. Because this is an essential metabolic process, the urea cost is added to the animal's maintenance energy requirement, leaving less energy available to support growth, productive and reproductive functions.

Milk Fever or Parturient Paresis

Lactating animals may be afflicted with parturient paresis or milk fever. Milk fever is caused by a reduced blood calcium level. Reduced blood calcium also leads to poor muscle tone, and this may predispose cattle to DA, retained placenta, and mastitis (Goff, 2000). The drop in blood calcium is caused by a combination of three factors.

1. The drain on blood calcium imposed by milk production

2. The inability of the digestive system (because of reduced appetite) to deliver enough calcium to replace that which is used for lactation

3. The inability of the parathyroid gland to direct mobilization of stored calcium reserves

Blood calcium is normally maintained within a narrow range, even when dietary intake of calcium is inadequate to match the loss of calcium in milk. This is because the endocrine system is very sensitive to small changes in concentration of calcium in the blood. When serum calcium is low, the parathyroid gland secretes parathyroid hormone (PTH), which facilitates removal of calcium from bone. When serum calcium is high, the thyroid gland secretes calcitonin, which facilitates deposition of calcium in bone.

Milk fever occurs when blood calcium falls below the level necessary to support normal physiology. It usually occurs within 3 days of parturition. Cows stop eating and are unsteady on their feet. The eyes of affected animals are dull and the pupils are dilated. Fever is not a symptom of milk fever; in fact, body temperature may be subnormal. As the problem progresses, the animal will fall down and will be unable to rise. Cows may become comatose and will die if left untreated.

Controlling Milk Fever through Manipulation of the Dietary Cation-Anion Difference

According to Stewart's Theory (see Chapter 9), a solution must remain neutral. If an excess of negatively charged anions is added, the solution becomes acidic rather than negatively charged: the anions replace the O[H.sup.-] in the solution. A reduction in O[H.sup.-] concentration means an excess of [H.sup.+] or acid. If an excess amount of anions are fed and absorbed into the blood, the blood is at risk of becoming acidic. The body reacts by excreting acid, primarily through action of the kidneys. In addition, the body mobilizes stored cations to counteract the anions. The primary cation that the body has in storage is calcium in the bone. Calcium is mobilized from the bone through the action of the parathyroid gland's PTH. Another mineral that is important in this discussion is magnesium. Magnesium is essential for proper function of the PTH.

For cows that are unable to maintain blood calcium level through the transition period, a manipulation of the dietary cation-anion difference (DCAD) has been an effective prophylactic, provided the cow absorbs adequate magnesium. By feeding more anions (Table 18-2) and thereby reducing the cation-anion difference for the 2 weeks prior to freshening, the cow is put into a similar situation as she is in at calving. She is forced to mobilize the cation she has in storage, which is calcium. This means that the parathyroid gland is forced to secrete PTH prior to freshening. It is important that these cows be put on lactation diets with normal cation-anion difference levels immediately following freshening to prevent the withdrawal of excessive levels of calcium from bone.

In a sense, by reducing the DCAD of the diet, an idle parathyroid gland is toned up and readied for active duty. Dry-cow feeding programs that predispose transition cows to a "lazy" parathyroid gland are those with excess cations. The two cations that appear to be most important are calcium and potassium. The intake of calcium and potassium by dry cows should be restricted, depending on the incidence of transition cow problems. Overall intake of calcium should be limited to 50 to100 g per cow per day and potassium content of forages for dry cows should be less than 2 percent (Chase, 2001). High levels of potassium in dry-cow diets may also interfere with magnesium absorption. Buffers should not be fed to dry cows because buffers in the dry cow's rumen may create conditions that reduce the efficiency with which magnesium is absorbed.

Acidosis

Because fresh cows are likely to be on high-grain diets, acidosis is a potential problem during this period, although it could be a problem throughout the lactation. To avoid acidosis problems in dairy cows, the rumen pH should be maintained above 6.28. Acidosis is discussed in Chapter 20.

Milk-Fat Depression

Diets that result in a fall of rumen pH below 6.0 are associated with milk-fat depression in dairy cows (NRC, 2001). Milk-fat depression is a reduction in the normal fat component of milk. This may directly affect the market value of the milk, but it is also an indication that the rumen ecology is unsettled. The fat in the milk and tissues of ruminant animals is highly saturated, regardless of the type of fat in the diet. This is because--in the absence of oxygen--rumen microbes use available unsaturated fats as oxidizing agents. As unsaturated fatty acids become reduced or "biohydrogenated," they become saturated fatty acids. These saturated fatty acids are passed on to the small intestine where absorption takes place. In an acid rumen, the process of biohydrogenation is apparently altered, resulting in an increased microbial production of trans fatty acids (Chapter 8). These trans fatty acids made in the rumen are incorporated into milk fat, but apparently with reduced efficiency, resulting in milk-fat depression. Correction of milk-fat depression involves maintaining a rumen pH above 6.28 by feeding adequate forage. Dietary buffers are also helpful.

Prussic Acid Poisoning

Under certain conditions, some grasses, particularly forage sorghums, may accumulate hydrocyanic acid (prussic acid) in their tissues. Prussic acid poisoning is discussed in Chapter 20.

Tall Fescue Toxicosis

Dairy animals that consume pasture or hay containing tall fescue that has been infected with an endophyte are susceptible to tall fescue toxicosis, which has various effects on health, production, and reproduction. Tall fescue toxicosis is discussed in Chapter 24.

END-OF-CHAPTER QUESTIONS

1. What is a transition cow?

2. What does a high blood level of nonesterified fatty acids in transition cows indicate?

3. What class of compounds is produced as a result of the incomplete oxidation of NEFA by the liver? What should be the first management strategy to prevent ketosis?

4. Ketosis, fatty liver, DA, retained placenta, mastitis, and metritis are all problems that share the same root cause. What is it?

5. What ration component will do the most to stimulate rumen development in the young calf?

6. How should the BCS of cows at the end of their lactation compare to the BCS of cows when they calve?

7. Explain how feeding anionic salts can prevent milk fever.

8. What is the fate of unused protein in dairy cow diets? Give three negative consequences of feeding excess protein to dairy cows.

9. What are two effects of ionophore when fed to dairy animals?

10. What ration constituent is used in the formula that predicts rumen pH?

REFERENCES

Albright, J. L. (2001). Personal communication to R. J. Grant.

Annen, E. L., Collier, R. J., McGuire, M. A., & Vicini, J. L. (2004). Effects of dry period length on milk yield and mammary epithelial cells. Journal of Dairy Science. 87, E66-E76.

Bachman, K. C., & Schairer, M. L. (2003). Invited review: Bovine studies in optional lengths of dry periods. Journal of Dairy Science. 86, 3027-3037.

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Table 18-1
Products and modes of action
for additives that have been
used to prevent ketosis in
dairy cattle

Product                Mode of Action

Propylene glycol       Source of glucogenic precursors

Calcium propionate     Source of glucogenic precursors

Niacin                 Specific mode of action is unknown--involved
                         in energy metabolism. Reduces blood NEFA.

Conjugated linoleic    Reducing the fat content in milk, thereby
  acid                   reducing the need for energy

Choline                Specific mode of action is unknown-possibly
                         improves efficiency of gluconeogenesis in
                         liver

Monensin               Increases rumen production of propionate, a
                         glucogenic precursor.

Table 18-2
Important cations and anions
in animal nutrition

Cations     Anions

Sodium      Chloride
Potassium   Sulfur
Calcium     Phosphorus
Magnesium
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Author:Tisch, David A.
Publication:Animal Feeds, Feeding and Nutrition, and Ration Evaluation
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Date:Jan 1, 2006
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