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Unique Aspects a of Dairy JO Cattle Nutrition TRAN S ITION COWS AN D NONLACTATING COWS Nutritional and Physiologic Status of the Transition Cow Fetal dry weight increases exponentially during gestation (House and Bell, 1993; National Research Council, 19961. Bell et al. (1995) indicated linear or nonlinear regression models were more suitable than exponential models for describing increases in fetal dry weight, fresh weight, and crude protein (CP) and energy accretion during the final trimester of pregnancy. They speculated that exponential models might be more appropriate when describing fetal growth for the entire gestation (i.e., including periods when fetal size is very small). Because conceptus growth approaches linearity during the final stages of gestation, exponential models developed from data obtained through- out pregnancy may overestimate growth during late gesta- tion. Fetal sex does not influence growth rates (Ferrell et al., 1982; House and Bell, 19931. Fetal tissue accounts for 45 percent of the uterine dry weight at day 190 of pregnancy and 80 percent at day 270 of pregnancy (Bell et al., 19951. The dry period, in particular the transition period, is characterized by dramatic changes in endocrine status. These changes prepare the cow for parturition and lacto- genesis. Plasma insulin decreases and growth hormone increases as the cow progresses from late gestation to early lactation, with acute surges in plasma concentrations of both hormones at parturition (Kunz et al., 19851. Plasma thyroxine (T4) concentrations gradually increase during late gestation, decrease approximately 50 percent at calv- ing, and then begin to increase (Kunz et al., 19851. Similar but less pronounced changes occur with 3,5, 3'-triiodothy- ronine (TV. Estrogen, primarily estrone of placental origin, increases in plasma during late gestation but decreases immediately at calving (Chew et al., 19791. Progesterone concentrations during the dry period are elevated for main- tenance of pregnancy but decline rapidly, approximately 2 days before calving (Chew et al., 19791. Glucocorticoid and prolactin concentrations increase on the day of calving and return to near prepartum concentrations the following day (Edgerton and Hats, 19731. Changes in endocrine status and decreases in dry matter intake (DMI) during late gestation influence metabolism and lead to mobilization of fat from adipose tissue and glycogen from the liver. Plasma nonesterif~ed fatty acids (NEFA) increase two-fold or more between 2 to 3 weeks prepartum and 2 to 3 days prepartum, at which time the concentration increases dramatically until completion of parturition (Bertics et al., 1992; Vazquez-Anon, 1994; Grum et al., 19961. How much of the initial increase in plasma NEFA can be accounted for by changing endocrine status compared with energy restriction resulting from decreased DMI is not known. Force feeding cows during the prefresh transition period reduced the magnitude of NEFA increase, but did not completely eliminate it (Ber- tics et al., 19921. These observations indicate at least part of the prepartum increase in plasma NEFA is hormonally induced. The rapid rise in NEFA on the day of calving is presumably due to the stress of calving. Plasma NEFA concentrations decrease rapidly after calving, but concen- trations remain higher than they were before calving. Plasma glucose concentrations remain stable or increase slightly during the prefresh transition period, increase dra- matically at calving, and then decrease immediately post- partum (Kunz et al., 1985; Vazquez-Anon et al., 19941. The transient increase at calving may result from increased glucagon and glucocorticoid concentrations that promote depletion of hepatic glycogen stores. Although the demand for glucose by mammary tissue for lactose synthesis contin- ues after calving, hepatic glycogen stores begin to replete and are increased by day 14 postpartum (Vazquez-Anon et al., 19941. This probably reflects an increase in gluconeo- genic capacity to support lactation. Blood calcium decreases during the last few days prior to calving due to the loss of calcium for the formation of colostrum (Goff and Horst, 1997b). Plasma Ca concentra- tions are controlled by the coordinated actions of parathryr- oid hormone and 1, 25-dihydroxyvitamin D3. These hor- manes act on the intestine, kidney, and bone to increase blood calcium during the periparturient period. Adaptation 184

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of the intestine, kidney, and bone to higher demands for calcium takes several days so that blood calcium typically does not return to normal concentrations until several days postpartum (Goff and Horst, 1997b). As cows initiate and terminate the dry period, there are changes in rumen dynamics. These alterations are nutri- tionally induced rather than physiologically induced. Chan- ging from a diet that is high in concentrate to a diet that is high in fiber causes alterations in the microbial popula- tion and characteristics of the rumen epithelium. High concentrate diets favor starch utilizing bacteria that enhance propionate and lactate production; high fiber diets favor cellulolytic bacteria and methane production and discriminate against bacteria that produce propionate and utilize lactate. End products of fermentation influence papillae growth in the rumen (Dirksen et al., 19851. Papillae are responsible for the absorption of volatile fatty acids. Increasing grain in the diet and propionate concentration in the rumen favors elongation of papillae; diets high in fiber cause the papillae to shorten. As much as 50 percent of the absorptive area in the rumen may be lost during the first 7 weeks ofthe dryperiod and elongation of papillae after reintroduction of concentrate takes several weeks (Dirksen et al., 19851. Consequently, sudden introduction of grain immediately postcalving has several deleterious consequences. Lactate production increases prior to the re-establishment of lactate utilizing bacteria. Lactate is more potent in reducing ruminal pH than other volatile fatty acids and volatile fatty acids are absorbed at a faster rate when pH is low (Goff and Horst, 1997b). Rumen papillae will not have had sufficient time to elongate, there- fore, volatile fatty acid absorption is limited. During the transition period, the immunologic status of the cow is compromised. Neutrophil and lymphocyte function is depressed and plasma concentrations of other components of the immune system are decreased (Goff and Horst, 1997b). It is not known why immune function is suppressed but it may be related to the nutritional and physiologic status of the cow. Estrogen and glucocorticoids are immunosuppressive agents and they increase in plasma as parturition approaches (Goff and Horst, 1997b). Intake of vitamin A and E and other nutrients essential for immune function may be decreased as DMI is reduced during the periparturient period. Nutrient Requirements for Pregnancy Dry cows require nutrients for maintenance, growth of the conceptus, and perhaps growth of the dam. Estimation of the nutrient requirements for pregnancy by the factorial method requires knowledge of the rates of nutrient accre- tion in conceptus tissues (fetus, placenta, fetal fluids, and uterus) and the efficiency with which dietary nutrients are Unique Aspects of Dairy Cattle Nutrition 185 utilized for conceptus growth. There are limited data for dairy cattle. Estimates of CP, energy, and most mineral requirements for gestation during the last two months of pregnancy are from House and Bell (1993) and Bell et al. (19951. Rates of growth and chemical composition were measured in multiparous Holstein cows that were serially slaughtered from 190 to 270 days of pregnancy. Requirements derived from these studies and equations used for the model are discussed in chapters 2 (energy), 5 (protein), and 6 (minerals). Other estimates for energy and crude protein require- ments are available, but they were obtained from beef cattle, dairy breeds other than Holsteins, or from research conducted more than 25 years ago. However, estimates from Bell et al. (1995) do not vary greatly from previous estimates and thus are supportive of requirements pub- lished in Nutrient Requirements of Dairy Cattle (National Research Council, 19891. Additionally, by using the data from Bell et al. (1995) energy, protein, and mineral require- ments for pregnancy were all derived from the same study. A quadratic regression equation best described protein and energy accretion in the gravid uterus. Estimates of CP and energy requirements to support pregnancy were derived from cows with a mean body weight of 714 kg that carried a single fetus. They are a function of day of gesta- tion, but an adjustment to accommodate differences in calf birth weight was added to the equations derived from Bell et al. (19951. Crude protein requirements for gestation were obtained by assuming an efficiency of 0.33 for conver- sion of metabolizable protein (MP) to conceptus protein and efficiency of 0.7 for conversion of dietary CP to MP (Bell et al., 19951. The efficiency of conversion of MP to conceptus protein has been reduced from 0.5 used in the previous edition (National Research Council, 19891. The efficiency of conversion of metabolizable energy to concep- tus net energy (NE) was assumed to be 0.14 (Ferrell et al., 19761. The low efficiency most likely reflects the high cost of maintaining the fetus. Nutrient Intake Intake of nutrients is a function of DMI and nutrient density of the diet. Dry matter intake during the final 21 days of gestation was described (Hayirli et al., 1998) by an exponential function: y = a + pxekxt where y = DMI as a percentage of body weight, a = the asymptotic inter- cept at time = oo (minus infinity), p = the magnitude of intake depression (kg) from the asymptotic intercept until parturition, and edit describes the shape of the curve. Time (t) is expressed as: days pregnant280. Following evaluation of the model (mean square predicted error = 0.06 percent BW2, mean bias = 0.01 percent BW when plotting mean daily observed DMI versus mean daily pre-

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186 Nutrient Requirements of Dairy Cattle dieted DMI), the original data set and the data set used for evaluation were combined to generate the following prediction equations for DMI during the final 21 days of gestation: Heifers: DMI (% of BW) = 1.71 - 0.69e35t (9-1) Cows: DMI (% of BW) = 1.97 - 0.75e~6t (9-2) These equations were from a data set that included 172 heifers and 527 cows used in 16 experiment treatments that were conducted at 8 universities and involved 49 treatments. Factors that influence prepartum DMI are not well established. Zamet et al. (1979a) reported lower prepartum DMI for cows diagnosed with fat cow syndrome compared with "normal" cows that did not have postpartum complica- tions. Hayirli et al. (1998) indicated that over conditioned cows experience a gradual decline in DMI during the pre- fresh transition period whereas thin cows maintain DMI longer prior to experiencing a more abrupt decrease in DMI shortly before calving. However, a relationship between body condition and prepartum DMI does not imply cause and effect. Categorization of cows on the basis of body condition may also categorize cows into groups that have many genetic, physiologic, and biochemical differences. Ration composition and nutrient content may influence prepartum DMI. Increasing energy (Coppock et al., 1972; Hernandez-Urdaneta et al., 1976; Minor et al., 1998) or energy and protein (VandeHaar et al., 1999) content of the diet during the prefresh transition period resulted in higher dry matter (DM) and energy intake. In contrast, replacement heifers fed 35 percent concentrate during the final 5 months before first calving had lower DMI (but similar energy intake) during the final 10 days prepartum than did cows fed 6 percent concentrate during the same period (Grummer et al., 19951. The blood concentrations of many hormones increase or decrease dramatically at parturition and may be potent modifiers of DMI. For example, plasma estrogen of placen- tal origin (specifically estrone) increases in blood as parturi- tion approaches. Exogenous estrogen administration inhib- its DMI (Grummer et al., 19901. Reduced DMI during estrus and late pregnancy may reflect greater endogenous estrogen production. Development of metabolic disorders during the transi- tion period may cause a reduction in DMI. Cows with hypocalcemia have lower prepartum DMI (Goff and Horst, 1997b). Hypocalcemia may cause loss of muscle tone that could adversely affect rumen function, intestinal peristalsis, and passage rate of digesta. Slower passage rates may have a negative effect on DMI. Energy and Protein Density for Dry Cow Diets Table 6-5 of Nutrient Requirements of Dairy Cattle (National Research Council, 1989) listed one set of nutrient density recommendations for dry, pregnant cows. In the current edition, separate nutrient density guidelines have been developed for far-off dry cows and prefresh transition cows (Chapter 141. This gives greater recognition to DMI depression prior to calving and the unique physiologic and nutritional changes that are associated with late pregnancy, parturition, and lactogenesis. Formulation of a unique diet for prefresh transition cows should reduce the risk of meta- bolic disorders during early lactation and improve lactation performance. Nutrient density guidelines for dairy cattle can be obtained by dividing nutrient requirements as determined by the factorial method by predicted DMI. While this approach is appropriate for most classes of cattle, it is problematic for prefresh transition dairy cows because DMI and nutrient requirements are changing relatively rapidly during late gestation. Clearly it is not practical to constantly reformulate diets on a daily basis as cows prog- ress through the prefresh transition period. Additionally, animal physiology at parturition, microbial ecology of the rumen, and pharmacologic effects of nutrients also must be considered when deriving nutrient density recommen- dations for transition cows. Unique considerations for feed- ing protein and energy are described below; discussion of adjustments for other nutrients can be found in appropriate sections within this chapter (e.g., selenium/retained pla- centa, calcium/milk fever). PROTEIN Results obtained by dividing CP requirements for main- tenance, growth (heifers only), and gestation (Bell et al., 1995; data in this edition) by predicted DMI are shown by the solid lines in Figure 9-1. Using this approach, it appears that CP content could be 12 percent or slightly less for mature cows during all but the last few days of the dry period. The previous edition established a minimum of 12 percent CP for diets of dry cows (National Research Council, 19891. Justification for establishing a minimum of 12 percent was absent. Presumably this was based on a minimum amount of CP believed to be necessary to opti- mize some aspect of ruminal function (e.g., microbial pro- tein synthesis or fiber digestion) (Sahlu et al., 19951. In this revision, it has been established that prefresh transition diets should not be formulated to contain less than 12 percent CP. Feeding a diet containing 12 percent CP pro- vides a margin of safety in the event that DMI would be lower for low protein diets. Chew et al. (1984) fed approximately 9 or 11 percent CP during the entire dry period and observed higher prepartum DMI and higher milk yields when feeding the higher protein diet. Feeding diets with 12 percent CP at predicted DMI is insufficient to meet protein requirements for heifers during the transti- tion period (Figure 9-11. Heifers have lower DMI as a

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Unique Aspects of Dairy Cattle Nutrition 187 Heifer (-mammary) Cow (-mammary) --a- Heifer(+mammary) --a- Cow(+mammary) 20.00 16.00 c: 12.00 - 8.00 - 4.00 - 0.00 ---- -- ----~--~--------~-~--'~'~''-''~''~''Wo i: = , lllllllllllllllllll -19 -17 -15 -13 -11 -9 -7 -5 -3 -1 Day Relative to Calving FIGURE 9-1 Dietary concentrations of crude protein needed in diets fed to transition cows to meet requirements. Values were calculated assuming dry matter intakes as predicted by the exponential model described in the text. Solid lines represent calculations using estimates of CP requirements for maintenance, growth, and gestation (from this edition) for a 740 kg mature cow or a 615 kg replacement heifer. Dotted lines represent calcu- lations using estimates of requirements for maintenance, grog, gestation (from this edition), and mammary growth (130 g/d, see text). Body condition score = 3.3, calf birth weight = 45 kg, and heifer growth rate = 300 g/d (without conceptus). Diet consisted of 35 percent corn silage, normal; 34 percent grass silage, C-3, mid-maturity; 10 percent corn grain, ground high moisture; 8 percent soybean meal, solvent, 48 percent CP and 13 percent beet, sugar pulp. percentage of body weight and have additional nutrient requirements for growth. A preliminary report (Santos et al., l999a,b) indicated that primiparous but not multipa- rous cows have improved lactation performance when the CP in prepartum diets is increased from 12.7 to 14.7 per- cent by the addition of animal proteins. Crude protein requirements for mammary growth were not included in the model. Insufficient data for mammary parenchymal growth rates, mammary composition, and efficiency of conversion of MP to net protein during late gestation were available to accurately predict requirements for mammary growth. However, as outlined by VandeHaar and Donkin (1999), if mammary parenchymal mass increases by 460 g/d during the transition period (Capuco et al., 1997), mammary parenchymal tissue is 10 percent crude protein (Ferrell et al., 1976; Swanson and Poffenbarger, 1979), and efficiencies of conversion of dietary CP to MP and MP to tissue net protein are 0.7 and 0.5 (National Research Council, 1996), then additional CP for mammary growth would be approximately 130 g/d. This would increase the dietary CP needed to meet requirements by approximately one percentage unit (dotted lines, Figure 9-11. Additional research is needed to determine protein and amino acid requirements for mammary growth. Several research trials have been conducted to examine the effects of dietary CP during the prefresh transition period on health and productivity of postpartum dairy cows. Increasing dietary CP beyond 12 percent during the dry period by addition of feeds that are high in ruminally unde- gradable protein improved reproductive performance of first lactation cows (Van Saun et al., 1993) and reduced the incidence of ketosis in multiparous cows (Van Saun and Sniffen, 19951. Increasing dietary CP by 2 to 4 percent- age units above 12 to 13 percent CP during the prefresh transition period has reduced postpartum feed intake (Crawley and Kilmer, 1995; Van Saun et al., 1995; Green- f~eld et al., 1998; Hartwell et al., 1999; Putnam et al., 1999) or milk yield (Crawley and Kilmer, 1995; Greenf~eld et al., 19881. Most studies have shown that milk yield is not influenced by protein content of prepartum diets (Van Saun et al., 1993, Van Saun and Sniffen, 1995; Wu et al., 1997; Putnam and Varga, 1998; Huyler et al., 1999; Putnam et al., 1999; VandeHaar et al., 19991. Although not observed in the majority of studies, milk protein yield (Moorby et al., 1996) and percentage (Van Saun et al., 1993; Moorby et al., 1996) have been increased when feeding additional ruminally undegradable protein prepartum. Cows fed diets containing 10.5, 12.6, or 14.5 percent CP were all in posi- tive nitrogen balance during the prefresh transition period and had similar lactation performance when fed identical diets postpartum (Putnam and Varga, 19981. Strategic sup- plementation of limiting amino acids may prove to be more successful than increasing total CP or ruminally undegrad- able protein; however, amino acid requirements for preg- nancy have not been defined. A preliminary report (Cha- lupa et al., 1999) did not indicate a benefit of feeding ruminally protected amino acids during the prefresh transi- tion period; milk and protein yields were increased when supplementation occurred during the postpartum or pre- partum and postpartum period. Although some positive results have been noted when increasing CP beyond 12 percent by feeding additional ruminally undegradable protein, the results have been inconsistent and sometimes negative (e.g., reduced feed intake). The capacity of the cow to detoxify ammonia may be limited during the periparturient period (Strang et al., 19981. Feeding excess protein may be detrimental to the environment. At this time, there is insufficient evidence to support feeding diets with more than 12 percent CP to mature cows during the prefresh transition period. There- fore, the recommendation of 12 percent CP for dry cow diets that was made in the last edition (National Research Council, 1989) has been retained for mature cows (Table 14-111. Heifers may benefit from feeding higher amounts of CP. According to Figure 9-1, average CP density needed in prefresh transition diets to meet requirements at pre- dicted feed intakes would be 14.2 percent if an adjustment is made for mammary growth. Therefore, it is recom-

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188 Nutrient Requirements of Dairy Cattle mended that heifers be fed diets containing 15 percent CP during the prefresh transition period (Table 14-101. Further research is required to more clearly define protein and amino acid requirements during the prefresh transi- tion period. ENERGY The recommended energy density for diets fed to dry cows was 1.25 Mcal NE/kg DM in Table 6-5 of Nutrient Requirements of Dairy Cattle (National Research Council, 19891. Assuming DMI as predicted above, 1.25 Mcal NE/kg DM appears adequate for meeting the energy requirements of cows during the far-off dry period but becomes inadequate during the final one to two weeks of the prefresh transition period depending on whether an adjustment has been made for mammary growth (Figure 9-21. Heifers have lower DMI and additional energy requirements for growth, therefore, 1.25 Mcal NE/kg DM is inadequate during the entire prefresh transition period. The recommendation for energy density in diets fed to prefresh transition cows and heifers is 1.62 Mcal NE/kg DM (Tables 14-1O, 14-111. At predicted dry matter intakes, 1.62 Mcal NE/kg DM will not provide sufficient energy to meet requirements of heifers during a significant portion 2.5or 2.00 - 1 .50 - z 1.00- 0.50 - 0.00 - Heifer (-mammary) ~ Heifer (+mammary) Cow (-mammary) o Cow (+mammary) 0--O--O-.O.-O.-0.-O.0.O--c~~v~ j , , , , , , , , j 19 17 15 13 11 9 7 Day Relative to Calving j j , j `2 1 J ~ 1 FIGURE 9-2 Dietary concentrations of NED needed in diets fed to transition cows to meet requirements. Values were calculated assuming dry matter intakes as predicted by the exponential model described in the text. Solid lines represent calculations using estimates of NED requirements for maintenance, growth, and gestation (from this edition) for a 740 kg mature cow or a 615 kg replacement heifer. Dotted lines represent calculations using estimates of requirements for maintenance, growth, gesta- tion (from this edition), and mammary growth (3Mcal/d, Vane- Haar et al., 1999~. Body condition score = 3.3, calf birth weight = 45 kg, and heifer growth rate = 300 g/d (without conceptus). Diet consisted of 35 percent corn silage, normal; 34 percent grass silage, C-3, mid-maturity; 10 percent corn grain, ground high moisture; 8 percent soybean meal, solvent, 48 percent CP and 13 percent beet, sugar pulp. of the prefresh transition period and possibly of mature cows during the final few days prior to calving. However, it is recommended not to feed diets with greater than 1.62 Mcal NE L/kg DM (Tables 14-1O, 14-11) because feeding more energy dense diets may increase intake of rapidly fermentable carbohydrate too quickly and adversely affect ruminal fermentation and DMI. Feeding diets with 1.62 Mcal NE/kg DM will probably provide more energy than required for maintenance and gestation for the majority of the prefresh transition period for cows in the 2n~ or greater gestation. However, there are several reasons why feeding diets that high in energy could be beneficial. Increasing energy density by increasing nonf~ber carbohy- drate will allow ruminal microorganisms to adapt to the high concentrate diets that will be fed postpartum. Greater volatile fatty acid production in the rumen will stimulate papillae growth and increase the capacity for acid to be absorbed from the rumen when additional grain is fed postpartum (Dirksen et al., 19851. Increased propionate formation may trigger an insulin response, which can act to reduce fatty acid mobilization from adipose tissue and lipid-related metabolic disorders (Grummer, 1993; Grum- mer, 19951. Finally, energy requirements for mammary growth have not been described and were not considered when determining total energy requirements for prefresh transition cows. Feeding diets with 1.62 Mcal NE/kg DM would probably accommodate energy requirements for maintenance, pregnancy, and mammary growth in mature cows (VandeHaar et al., 1999) except for the final few days prior to calving. ETIOLOGY AND NUTRITIONAL PREVENTION OF METABOLIC D I S O R D E R S Fatty Liver and Ketosis Fatty liver and ketosis are most likely to occur during periods when blood NEFA concentrations are elevated. The most dramatic elevation occurs at calving when plasma concentrations often exceed 1000 ~eq/L (Bertics et al., 1992; Vazquez-Anon et al., 1994; Grum et al., 19961. Uptake of NEFA by liver is proportional to NEFA concen- trations in blood (Bell, 1979). Extensive reviews on regula- tion of hepatic lipid metabolism and its relation to fatty liver and ketosis have been published recently (Emery et al., 1992; Grummer, 1993; Bauchart et al., 1996; Drackley, 1999; Hocquette and Bauchart, 1999) and will not be detailed here. Briefly, nonesterif~ed fatty acids taken up by the liver can either be esterif~ed or oxidized in the mitochondria or peroxisomes (Drackley, 19991. The pri- mary esterif~cation product is triglyceride. Triglyceride can either be exported as part of a very low density lipoprotein

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Unique Aspects of Dairy Cattle Nutrition 189 or be stored. In ruminants, export of triglyceride occurs at a very slow rate relative to many other species (Kleppe et al., 1988; Pullen et al., 19901. Therefore, under condi- tions of elevated hepatic NEFA uptake (e.g., low blood glucose and insulin) fatty acid esterif~cation and triglyceride accumulation occurs. The cause for the slow rate of triglyc- eride export from the liver of ruminants is not known. Complete oxidation of NEFA leads to the formation of CO2; incomplete oxidation yields ketones, primarily acet- oacetate and beta-hydroxybutyrate. Ketone formation is also favored when blood glucose and insulin concentrations are low, partially because of greater fatty acid mobilization from adipose tissue. Low insulin probably enhances fatty acid oxidation by decreasing hepatocyte malonyl-CoA con- centrations and sensitivity of carnitine palmitoyltransfer- ase-1 to malonyl-CoA (Emery et al., 19921. Carnitine palmi- toyltransferase-1 is responsible for translocating fatty acids from the cytosol to the mitochondria for oxidation and is inhibited by malonyl-CoA. Propionate is antiketogenic. The antiketogenic properties of propionate are likely due to indirect effects as an insulin secretegogue as well as direct effects on hepatic metabolism (Grummer, 19931. Ketonemia is common at calving during the sudden surge in NEFA, when energy requirements for milk production far exceed energy intake, and as a secondary disorder to others that may cause DMI depression and elevated NEFA. Elevated liver triglyceride concentration is common in cows immediately after parturition suggesting that mea- sures to prevent fatty liver take place during the prefresh transition period (Grummer, 19931. Fatty liver can be a secondary complication to any disorder that causes a cow to experience negative energy balance. Because of the slow rate of triglyceride export as lipoprotein, once fatty liver has developed, it will persist for an extended period of time. Depletion usually commences when the cow reaches positive energy balance and may take several weeks until completion. Ketosis usually occurs 2 to 4 weeks postpar- tum; reasons for the lag period between fatty liver and ketosis are not known. However, cows with elevated liver triglyceride and depressed glycogen are most susceptible to ketosis, and fatty liver preceded ketosis when ketosis was experimentally induced (Veenhuizen et al., 19911. Fatty acid oxidation and ketogenesis are likely the major routes of depletion of excess fat from the liver. Ketones may inhibit fatty acid mobilization from adipose tissue and ultimately reduce hepatic fatty acid uptake and triglyceride accumulation (Emery et al., 19921. Reducing severity and duration of negative energy bal- ance is crucial in the prevention of fatty liver and ketosis. The critical time for the prevention of fatty liver is approxi- mately one week prior to calving through one week after parturition (Grummer, 19931. This is when the cow is most susceptible to development of fatty liver, which is an indica- tor of ketosis. Maximizing DMI during the week prior to and after calving may be achieved by avoiding overconditi- oned cattle, rapid diet changes, unpalatable feeds, peripar- turient diseases, and environmental stress. Effects of body condition score on health and productivity are variable; however, extremely thin or overconditioned cows should be avoided. Thin cows (body condition score ' 3) can be fed additional energy during the dry period to replenish condition without causing fatty liver because the liver is not a lipid depot during positive energy balance. Over conditioned cattle (body condition score ~ 4) should not be feed restricted as this will promote fat mobilization from adipose tissue and elevate blood NEFA and liver triglyceride. Compounds to decrease fatty acid mobilization from adipose tissue or increase lipoprotein export from the liver have been suggested for prevention of fatty liver and keto- sis. Feeding 3 to 12 g niacin per day may reduce blood ketones (Dufva et al., 1983) but a benef~cial effect on liver triglyceride concentration has not been observed (Skaar et al., 1989; Minor et al., 19981. Glucose or compounds that can be converted to glucose may decrease blood ketones following intravenous administration (Hamada et al., 19821. The response is presumably mediated via insulin, which suppresses fatty acid mobilization from adipose tissue. Pro- pylene glycol is a glucose precursor that can be given as an oral drench to reduce blood nonesterif~ed fatty acids and the severity of fatty liver at calving (Studer et al., 1993) or blood ketones postcalving (Sauer et al., 19731. Salts of propionic acid are also a glucose precursor and may be effective in lowering blood ketones when fed (Schultz, 19581. There is insuff~cient evidence to support the use of compounds that are known to be lipotropic agents in nonruminants (e.g., choline, inositol, and methionine) to prevent or treat fatty liver or ketosis (Grummer, 19931. Udder Edema Udder edema is a periparturient disorder characterized by excessive accumulation of fluids in the intercellular tis- sue spaces of the mammary gland. In severe cases, edema and congestion occur in the udder and umbilical area, and may be prominent in the vulva and brisket. Typically the incidence and severity are greater in pregnant heifers than in cows (Zamet et al., 1979; Erb and Grohn, 1988), and tend to be more severe in older than younger heifers (Hays and Albright, 19661. Udder edema can be a major discom- fort to the animal and causes management problems such as diff~culty with milking machine attachment, increased risk of teat and udder injury, and mastitis. Severe udder edema may reduce milk production and cause a pendulous udder (Dentine and McDaniel, 19841. The exact causets) of udder edema is unknown, more likely it is a multi-factorial condition. Restriction or stasis

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190 Nutrient Requirements of Dairy CattIe of venous and lymph flow from the udder in late pregnancy due to fetal pressure in the pelvic cavity, or increased blood flow to the udder without the concomitant increase in flow from the udder, causing increased venous pressure may be contributing factors (Vestweber and Al-Ani, 1983; Al- Ani and Vestweber, 19861. Changes in amounts and relative proportions of steroid hormones during late pregnancy may be involved, but are not well understood (Mavlen et al., 1983; Miller et al., 19931. Reduced concentrations of pro- teins and especially globulins in blood, suggesting an increase in vascular permeability as animals approach calv- ing, were associated with greater incidences of udder edema (Vestweber and Al-Ani, 19841. Other potential causes such as inheritance and dietary factors have been associated with the condition (Al-Ani and Vestweber, 19861. The remaining discussion focuses on possible con- tributing nutritional factors. 1- HIGH CONCENTRATE (GRAIN) FEEDING PREPARTUM Many early studies showed no effects of concentrate feeding prepartum on udder edema regardless of parity (Fountaine et al., 1949; Greenhalgh and Gardner, 1958; Schmidt and Schultz, 19591. However, Hathaway et al. (1957) and HemLen et al. (1960) reported increased sever- ity of edema in cows fed greater amounts of concentrate before parturition. Emery et al. (1969) found increased udder edema in pregnant heifers fed 7 to 8 kg of concen- trate/head per day compared with no concentrate during the last 3 weeks of gestation. Udder edema was not found in multiparous cows. Greenhalgh and Gardner (1958) observed no increase in the severity of udder edema in heifers fed 4 kg of concentrate/head per day. Effects of prepartum concentrate feeding on udder edema in multi- parous cows are less well documented. In one study, cows fed diets composed primarily of corn and alfalfa silages (88 percent of diet, dry basis) plus 12 percent high moisture corn, or 53.5 percent silages plus 46.5 percent high mois- ture corn had more edema and mastitis than cows fed an all hay diet for 30 days prepartum (Johnson and Otterby, 19811. Overall, the degree of influence of concentrate feed- ing on udder edema is unclear and a biologic mechanisms has not been elucidated. The possibility of influence of other nutrients (e.g., minerals) present in some concentrate mixes should not be overlooked. Obese cows may be more predisposed to udder edema (Vigue, 19631. Different concentrations of dietary protein, fed for the last 60 days of gestation did not affect incidence of udder edema, but the severity was greater in heifers than in cows (Wise et al., 19461. MINERALS It was suggested that increased edema observed in heif- ers in the study of Emery et al. (1969) resulted from 1 percent trace mineralized salt in the grain mix rather than increased concentrate feeding. Excessive intakes of sodium and potassium were implicated as causative agents in udder edema (Randall et al., 1974; Conway et al., 1977; Sanders and Sanders, 1981; [ones et al., 19841. Restriction of sodium chloride and water intakes reduced the severity and incidence of udder edema in pregnant heifers (HemLen et al., 19691. Lower incidence and severity of udder edema were found when diets contained no supplemental salts of sodium or potassium (Randall et al., 19741. In a field study of two commercial dairy herds, potassium fertilization to improve alfalfa production was implicated as the cause of increased udder edema (Sanders and Sanders, 19811. Cows consumed about 450 g of potassium/head per day. In an earlier controlled study, consumption of 454 g of a combi- nation of sodium and potassium chlorides increased the incidence and severity of udder edema (Randall et al., 19741. In a second study, the incidence and severity of udder edema were compared in pregnant heifers fed a grain mix containing 1 percent sodium chloride versus a grain mix with 4 percent supplemental potassium chloride plus 1 percent sodium chloride for 20 days with ad libitum intake of alfalfa hay. The mix with potassium chloride had no influence on the severity of udder edema (Randall et al., 19741. Chronic udder edema also was associated with anemia and hypomagnasemia (Hicks and Pauli, 19761. Overall, evidence supports the idea that excessive intake of the chloride salts of sodium or potassium increases the severity of udder edema, especially in late pregnant heifers. Intake of these salts typically can be controlled in the peripartum period. Evaluation of other salts of sodium (e.g., sodium bicarbonate) as they might affect the severity of udder edema was not reported. However, Nestor et al. (1988) reported that the severity of udder edema was greater when pregnant heifers were fed additional potas- sium bicarbonate (0 versus 272 g/head per day) or sodium chloride (23 versus 136 g/head per day) separately, but not when both salts were fed together. Utilizing forages and other feeds that contain low basal concentrations of potas- sium and sodium would be prudent if udder edema is prevalent. Tucker et al. (1992) and Lema et al. (1992) studied the effects of calcium chloride, a so-called anionic salt with diuretic properties, on incidence and severity of udder edema. Calcium chloride was used to reduce the cation- anion difference of the prepartum diet of primiparous and multiparous cows. In one study, udder edema was not reduced by supplementation of calcium chloride in the prepartum period, but edema tended to regress more quickly in the early postpartum period, especially in pri- miparous cows compared with multiparous cows. In a sec- ond study, pregnant heifers were fed similar basal diets supplemented with either calcium chloride (1.5 percent, dry basis) or calcium carbonate (2.17 percent) for 3 weeks

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- - ~ 1 1 . r 1 prepartum. Calcium chloride reduced udder edema most during the first week of feeding. The effect was less but still evident the last 2 weeks before calving. Onset and creve~opment ot ecrema were more gradual in heifers fed calcium chloride prepartum. When animals were fed the same calcium chloride supplemented diet after parturition (without prepartum feeding of calcium chloride), udder edema was greater at 2 weeks postpartum for heifers fed calcium chloride versus calcium carbonate fed prepartum. OXIDATIVE STRESS Oxidative stress of mammary tissues resulting from reac- tive oxygen metabolites may play a role in udder edema (Mueller et al., 1989a; Miller et al., 1993; Mueller et al., 19981. Excessive reactive oxygen metabolites (e.g., super- oxide and hydrogen peroxide) generated from increased metabolic activity, or for example, excessive exposure to aflatoxins, can initiate abnormal oxidative reactions causing peroxidation of lipids; damage to proteins, polysaccharides, and DNA; degeneration of integrity of cell walls and con- tents; and tissue damage. Reactive oxygen molecules by themselves are not reactive enough to cause peroxidative chain reactions, but conversion to even more reactive free radicals can be triggered by transition elements such as iron (a pro-oxidant). Release of catalytic iron occurs under conditions of stress, trauma, or nutritional imbalance. Zinc may protect against the catalytic action of iron. Sources of endogenous molecules (e.g., transferrin, lac- toferrin, ceruloplasmin, serum albumin, antioxidant enzymes, and glutathione) and exogenous antioxidants (e.g., p-carotene and ~x-tocopherol) are important to reduce excessive oxidation. Presumably the diet must sup- ply adequate ~x-tocopherol (vitamin E) as a chain-breaking antioxidant, copper, zinc, and manganese for superoxide dismutase, selenium for glutathione peroxidase, zinc to displace catalytic iron, and magnesium and zinc to stabilize membranes and maintain cellular integrity. Mueller et al. (1989b) evaluated the effectiveness of supplemental vitamin E to reduce severity of udder edema in pregnant heifers. Udder edema during the f~rst week after calving was less in heifers supplemented for 6 weeks before calving with 1000 IU vitamin E/head per day versus none. In another study, late pregnant heifers were fed factorial combinations of vitamin E L0 or 1000 IU/head per day], zinc L0 or 800 mg/head per day (about 90 ma/ kg)], and iron L0 or 12 g/head per day (about 1300 ma/ kg)~. When effects were compared regardless of dietary iron concentration, supplemental vitamin E reduced sever- ity of udder edema, but zinc did not. However, when iron was excessive, vitamin E was ineffective in reducing the severity of udder edema, but zinc was somewhat effective. It is believed that vitamin E and zinc may complement each other in antioxidant function. Unique Aspects of Dairy CattIe Nutrition 191 Nutritional defense against oxidative stress likely is sup- plied by supplementation of dietary antioxidants fed to meet nutrient requirements (Mueller et al., 19981. More research evaluating effects of oversupply of pro-oxidants in the diet and (or) supplementation of antioxidants in excess of nutrient requirements would be helpful to under- stand the effects of oxidative stress on udder edema and potential for its prevention. Milk Fever OCCURRENCE Milk fever affects about 6 percent of the dairy cows in the United States each year, according to the 1996 National Animal Health Monitoring Survey (USDA, 19961. In these cows the calcium homeostatic mechanisms, which normally maintain blood calcium concentration between 9 and 10 mg/dl, fail and the lactational drain of calcium causes blood calcium concentration to fall below 5 mg/dl. This hypocal- cemia impairs muscle and nerve function to such a degree that the cow is unable to rise. Intravenous calcium treat- ments are used to keep the cow with milk fever alive long enough for intestinal and bone calcium homeostatic mechanisms to adapt. Although milk fever is relatively easy to treat, cows that have had milk fever are more susceptible to other disorders such as mastitis (especially coliform), displaced abomasum, retained placenta, and ketosis (Curtis et al., 19831. Though milk fever affects only a small percent- age of cows, nearly all cows experience some decrease in blood calcium (hypocalcemia) during the f~rst days after calving, while their intestines and bones adapt to the cal- cium demands of lactation. This sub-clinical hypocalcemia contributes to inappetance in the fresh cow and predis- poses the cow to develop other diseases such as ketosis, retained placenta, displacement of the abomasum, and mastitis. Efforts made to raise the concentration of calcium in the blood of the fresh cow can benef~t milk production even in herds that do not seem to have a milk fever problem (Beede et al., 19911. ETIOLOGY AND PATHOGENESIS Milk fever is characterized by and the result of severe hypocalcemia (Oetzel and Goff, 19981. Hypophosphatemia (see phosphorus section in chapter 6) and hypomagnesemia also can be present and can be complicating factors in some cases. The degree of hypocalcemia experienced will depend on the amount of calcium leaving the extracellular calcium pool and the rate at which the calcium homeostasis system can replace that calcium loss. The adaptation to the onset of lactation during the critical first days of lactation is accomplished by release of parathyroid hormone (PTH), which reduces urinary calcium losses, stimulates bone cal-

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192 Nutrient Requirements of Dairy Cattle cium resorption, and increases 1,25-dihydroxyvitamin D synthesis to enhance active intestinal transport of calcium. All three must be operational if hypocalcemia is to be minimized. Milk fever risk factors reduce the efficiency of one or more of these homeostatic mechanisms. An important determinant of the risk for milk fever is the acid-base status of the cow at the time of parturition (Craige, 1947; Ender et al., 19711. Metabolic alkalosis impairs the physiologic activity of PTH so that bone resorp- tion and production of 1,25-dihydroxyvitamin D are impaired reducing the ability to successfully adjust to the calcium demands of lactation (Block, 1984; Block, 1994; Gaynor et al., 1989; Goff et al., 1991; Phillippo et al., 19941. Evidence suggests that metabolic alkalosis induces conformational changes in the PTH receptor, which pre- vents tight binding of PTH to its receptor. Cows fed diets that are relatively high in potassium or sodium are in a relative state of metabolic alkalosis, which increases the likelihood that they will not successfully adapt to the cal- cium demands of lactation and will develop milk fever. The parathyroid glands recognize the onset of hypocal- cemia and secrete adequate PTH. However, the tissues respond poorly to the PTH, leading to inadequate osteo- clastic bone resorption and renal 1,25-dihydroxyvitamin D production (Goff et al., 1991; Phillippo et al., 19941. This is particularly evident in cows that have been treated for milk fever and require further treatments due to reappear- ance (relapse) of milk fever signs. These cows have very high blood PTH concentrations but produce little 1,25- dihydroxyvitamin D at parturition. Full recovery from milk fever occurs only after the cow has responded to the PTH by producing 1,25-dihydroxyvitamin D. Production of 1,25- dihydroxyvitamin D can be delayed for 24 to 48 hours in some cows (Goff et al., 19891. MILK FEVER RISK FACTORS Age Heifers almost never develop milk fever. The risk of a cow developing milk fever increases with age. Heifers generally produce less colostrum than older cows, which may reduce the calcium stress they experience at calving. More importantly, the bones of heifers are still growing. Growing bones have large numbers of osteoclasts present, which can respond to parathyroid hormone more readily than the bones of mature cows. Aged cows have fewer intestinal vitamin D receptors (Horst et al., 19901. Breed The Jersey and, to a lesser extent, the Swedish Red and White and Norwegian Red breeds are well known to have a higher incidence of milk fever. The reasons remain unclear. Colostrum and milk of Jersey cows have a higher content of calcium than that produced by Holsteins, which may place a relatively large calcium stress on the Jersey cows. In one study, Jersey cows had significantly fewer intestinal receptors for 1,25-dihydroxyvitamin D than did Holsteins (Goff et al., 19951. Fewer receptors may impair the ability of Jersey cows to maintain calcium homeostasis. NUTRITIONAL CONSIDERATIONS Dietary Cation-Anion Difference. Because metabolic alka- losis is an important factor in the etiology of milk fever it is important to prevent metabolic alkalosis. The reason the cow's blood is alkaline is because of high dietary cations, especially potassium. Cations are minerals with a positive charge and include potassium, sodium, calcium, and mag- nesium. If the cations in the feed are absorbed into the blood they cause the blood to become more alkaline. If dietary cations are not absorbed they do not affect blood pH (Stewart, 19831. Nearly all ofthe potassium and sodium in the diet is absorbed by cows, making these two elements very powerful alkalinizing cations. Calcium and magnesium are poorly absorbed from the diet of the dry cow so these cations are not strong alkalinizing agents. Dry cow diets that are high in potassium, sodium, or both alkalinize the cow's blood and increase the susceptibility for milk fever. Addition of potassium or sodium to the prepartal ration of dairy cows will increase the incidence of milk fever. Adding calcium (from 0.5 to 1.5 percent) to practical prepartal diets does not increase the incidence of milk fever (Goff and Horst, 1997a). Hypomagnesemia. A second common cause of hypocal- cemia and milk fever in the periparturient cow is hypomag- nesemia (van de Braak et al., 1987; Allen and Davies, 1981; Barber et al., 1983; Sansom et al., 19831. Low magnesium in blood can reduce PTH secretion from the parathyroid glands; and can alter the responsiveness of tissues to PTH by inducing confirmational changes in the PTH receptor and G-stimulatory protein complex (Rude et al., 1985; Rude et al., 1978; Littledike et al., 19831. Cows fed ade- quate dietary magnesium in the prepartal ration will be slightly hypermagnesemic the day after parturition. Blood magnesium concentrations below 2.0 mg/dl within 24 h after calving suggest inadequate dietary magnesium absorption (Goff, 1998b). PREVENTION OF MILK FEVER Adjustment of Dietary Cation-Anion Difference (DCADJ Equations to describe DCAD include (Na+ + K+)(Cl- + S-2) (Ender et al., 1971), (Na+ + K+ Cl-) (Mongin, 1981), and (Na+ + K+ + 0.15 Ca+2 + 0.15 Mg+2) (Cl- + 0.6 s-2 + 0 5 P-3) (Goff et al., 19971. The last equation assigns coefficients to the major dietary cations and anions based on their acidifying or alkalinizing poten- tial. To achieve a low DCAD prepartal ration to prevent

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Unique Aspects of Dairy Cattle Nutrition 193 hypocalcem recommended: ia, the following adjustments are Reduce Dietary Sodium and Potassium Removing potass- ium from the ration can present a problem as alfalfa, other legumes, and many grasses accumulate potassium within their tissues to concentrations that are well above that required for optimal growth of the plant if soil potassium is high. Corn, a warm season grass, is less likely to accumulate potassium and corn silage is often a practical foodstuff to use to reduce DCAD (Beede, 19921. Other agronomic options to reduce dietary potassium have recently been reviewed (Horst et al., 1997; Thomas, 19991. Add Anions to Induce Mild (CompensatedJ Metabolic Aci- dosis Landmark studies (Ender et al., 1971; Ender and Dishington, 1967; Block, 1984) demonstrated that addition of anions to the prepartal diet could prevent milk fever. Ammonium, calcium, and magnesium salts of chloride and sulfate have been successfully used as acidifying anion sources. Chloride salts are more acidogenic than sulfate salts (Goff et al., 1997; Oetzel, 1991; Tucker et al., 19911. Hydrochloric acid also has been successfully utilized as a source of anions for prevention of milk fever and is the most potent of the anion sources available (Ender and Dishington, 1967; Goff and Horst, 19981. Monitoring urine pH of cows during the week before parturition has proven an effective means of assessing effectiveness of anion addi- tion to the prepartal ration. In Holstein cows effective anion addition reduces urine pH to between 6.2 and 6.8 (Gaynor et al., 1989; Pardon, 1995; Oetzel and Goff, 19981. Using the equation favored by most nutritionists, (Na+ + K+ ~(Cl- + S -2) it is common to attempt to bring DCAD below zero mEq/kg diet to achieve proper acidification of the cow. These targets are not well defined and anions should be added in small increments to the dry cow ration until the proper urine pH is achieved. Urine pH can be assessed as quickly as 48 to 72 hours after a DCAD adjustment. Feeding 0.35 to 0.40 percent magnesium in prepartal rations prevents a decline in the concentration of magne- sium in the blood at parturition. These levels ensure that there is adequate magnesium in the rumen to utilize the passive absorption mechanism for magnesium across the rumen wall and not be reliant on active transport of magne- sium across the rumen wall, a process that may be inhibited by dietary potassium (Oetzel and Goff, 19981. Because there is no readily labile body store of magnesium, the daily intake of dietary magnesium must supply needs. These higher levels are needed to accommodate the decline in DMI occurring in the periparturient period (Goff, 1998b; Horst and Goff, 19971. Phosphorus require- ments are met by feeding 40 to 50 g of phosphorus/cow/ day. Less than 25 g/cow/day may lead to hypophosphatemia and the downer cow syndrome (Julian et al., 1977; Goff, 1998a; Cox, 19981. More than 80 g of phosphorus/cow/day may induce milk fever (Barton et al., 19871. The optimal prepartal dietary calcium concentration is not well defined. In one study, the incidence of milk fever was not different in cows fed 0.5 or 1.5 percent calcium in diets (Goff and Horst, 1997a). Other studies have suc- cessfully utilized diets providing more than 150 g of cal- cium/cow/day along with anionic salts to prevent hypocal- cemia (Oetzel, 1988; Beede et al., 19911. Very high concen- trations of dietary calcium (~1.0 percent calcium) may reduce DMI and animal performance (Miller, 19831. Very Low Calcium Diets to Prevent Milk Fever Diets providing less than 15 g calcium/cow/day and fed for at least 10 days before calving will reduce the incidence of milk fever (Goings et al., 1974; Boda, 19541. This concen- tration of calcium places the cow in negative calcium bal- ance, stimulating parathyroid hormone secretion prior to calving. This activates bone osteoclasts stimulating bone calcium resorption and activates renal tubules to resorb urinary calcium and begin producing 1,25-dihydroxyvita- min D prior to calving (Green et al., 19811. Thus at the onset of lactation these homeostatic mechanisms for cal- cium are active, preventing a severe decline in the concen- tration of calcium in the plasma of cows. In the United States, it is nearly impossible to formulate this type of diet. Diets consisting of as little as 35 to 45 g of calcium/day will meet the calcium requirement of cows and will not stimulate the parathyroid glands adequately and will not effectively prevent milk fever. Oral Calcium Drenches at Calving Oral administration of calcium at calving reduces the incidence of milk fever but carries a slight risk of inducing aspiration pneumonia (Poisson and Pehrson, 1970; Hallgren, 1955; Oetzel, 1993; Goff et al., 1996), and can be labor intensive. Exogenous Vitamin D and Parathyroid Hormone Earlier literature often recommended feeding or injecting massive doses (up to 10 million units) of vitamin D 10 to 14 days prior to calving to prevent milk fever (Hibbs and Pounden, 1955; Littledike and Horst, 19801. This will increase intesti- nal absorption of calcium and can help prevent milk fever. Unfortunately, the dose of vitamin D that effectively pre- vents milk fever is very close to the level that causes irre- versible metastatic calcification of soft tissues. Lower doses may actually induce milk fever because the high levels of 25-OH D and 1,25-dihydroxyvitamin D suppress PTH secretion and renal synthesis of endogenous 1,25-dihydrox- yvitamin D (Littledike and Horst, 19801. Treatment with 1,25-dihydroxyvitamin D and its ana- logues or parathyroid hormone prior to calving can be effective but the effective dose is close to the toxic dose

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194 Nutrient Requirements of Dairy Cattle and problems with timing of administration, withdrawal from treatment, and expense have not made these treat- ments practical (Bar et al., 1985; Goff and Horst, 1990; Goff et al., 19861. Grass Tetany Hypomagnesemic tetany is most often associated with cows in early lactation (milk production removes 0.15 g magnesium from the blood for each liter of milk produced) grazing lush pastures high in potassium and nitrogen and low in magnesium and sodium (Littledike et al., 19831. This is the most common situation and it is often referred to as Grass Tetany, Spring Tetany, Grass Staggers, or Lacta- tion Tetany. The clinical signs in affected cows will depend on the severity of the hypomagnesemia. The disease will progess more rapidly and tends to be more severe if accom- panied by hypocalcemia, which is often the case. Dairy cows are usually affected 1 to 3 weeks into lactation espe- cially if they are on pasture. Moderate hypomagnesemia (between 0.5 and 0.75 mmol/L or 1.1 and 1.8 mg/dl) is associated with reduced DMI, nervousness, and reduced production of milk fat and total milk. This can be a chronic problem in some dairy herds that often goes unnoticed. It also can predispose these animals to milk fever (Goff, 19981. Despite the importance of magnesium there is no hor- monal mechanism concerned principally and directly with magnesium homeostasis. Factors affecting magnesium transport across the rumen epithelium have been discussed in the section on magnesium requirements. PREVENTION If hypomagnesemic tetany has occurred in one cow in a herd, steps should be taken immediately to increase intake of magnesium to prevent further losses. Getting an additional 10 to 15 g of magnesium into each pregnant cow and 30 g of magnesium into each lactating dairy cow each day will usually prevent further hypomagnesemic tetany cases. The problem with prevention is getting the extra magnesium into the animal (Goff, 1998b). Most magnesium salts are unpalatable. Magnesium oxide is the most palatable, most concentrated, least expensive, and, unfortunately, least soluble source of magnesium. Magnesium is readily acceptable in grain concentrates. Including 60 g of magnesium oxide in just 0.5 to 1 kg of grain will be effective. However the expense of the grain and the problems associated with feeding concentrates to pastured cattle often make this option difficult to imple- ment (Goff, 1998b). Feeding ionophores (monensin, lasalocid) can improve activity of the sodium-linked magnesium transport system in the rumen, increasing magnesium absorption efficiency about 10 percent. However, ionophores are not approved for use in many of the animals they could benefit. Rumen boluses that release ionophores for up to 150 days have been developed to make delivery of ionophores to animals at pasture practical. Pasture foliage can be dusted with magnesium oxide (500 g of magnesium oxide/cow or 50 kg magnesium oxide/ hectare or 50 lb/acre) weekly during the period when cows are tetany prone. Adding 2.5-5 g/L or 10 to 20 lb/500 gal magnesium sulfate 7H2O (epsom salts) or magnesium chloride 6H2O to the drinking water can be an economic means of supplementing magnesium if cows have access to no other water supply as the addition of the salts can reduce palatability. Unfortunately cows grazing lush high moisture pasture rarely drink enough water to make this method effective on tetany prone pastures. Molasses licks and mineral blocks containing magnesium oxide and salt can help supply magnesium to animals at pasture if made readily available and if the animals learn to use the licks prior to parturition. A problem with many of these methods is that some cows in the herd may not voluntarily consume enough of the magnesium supplement and on some tetano- genic pastures cows that do not receive supplementation are often found dead (Goff, 1998b). Intraruminal magnesium releasing boluses and bullets have been developed, which remain in the reticulum and release low levels of magnesium (1 to 1.5 g) each day for periods of up to 90 days. A 100 g magnesium alloy rumen "bullet" that is 86 percent magnesium has been developed and releases about 1 g of magnesium/day. Some producers administer 2 to 4 bullets per cow. These devices do not supply enough magnesium to raise magnesium in the blood subsantially, though there may be situations where they prove successful despite the low supplementation achieved. Retained Placenta and Metritis Retained placenta (retained fetal membranes) is defined as failure of the fetal membranes to be expelled within 12 to 24 hours after parturition. Metritis, an inflammation or infection of the uterus, is often associated with retained placenta. In path analysis, retained placenta was associated directly with increased days to first service and risk of metritis when compared with cows that expelled their pla- centas within 24 hours. A1SO7 retained placenta was associ- ated indirectly with the greater occurrence of cystic ovaries, lower milk yield, and greater culling; all were mediated through metritis (Erb et al., 19851. Multiple physiologic and nutritional factors have been associated with or implicated as causes of retained placenta and metritis (Maas, 1982; Miller et al., 1993; Goff and Horst, 1997b). Dystocia in heifers increased the risk of retained placenta and metritis by 3 to 4 times (Erb et al.,

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condition score (Wagner et al., 19991. Reductions in DMI and greater body weight gain during mid to late lactation might be expected if cows are in positive energy balance, and ionophores cause an increase in the NE content of the diet. Knowlton et al. (1996a) observed a slight increase in DMI when feeding lasalocid. Ionophores could have a positive influence on DMI if cows are fed high concentrate diets and lactate production in the rumen is decreased (Nagaraja et al., 19811; however, lactate concentration was increased in the study of Knowlton et al. (1996b). Reproductive performance of lactating cows grazing pas- ture was not improved by ionophore supplementation in two large field trials (Abe et al., 1994; Lean et al., 1994; Hayes et al., 19961. Phipps et al. (1997b) indicated that reproductive performance was not improved during the first lactation but was improved when cows were fed iono- phores for a second lactation. Feeding ionophores may improve animal health. Increased propionate production and gluconeogenesis may spare amino acid catabolism and reduce fat mobilization from adipose tissue and ketone production by the liver. An increase in plasma glucose, decrease in plasma nones- terif~ed fatty acids, decrease in blood beta-hydroxybutyrate, or combinations of the above have been attributed to iono- phore feeding on several occasions (Saner et al., 1989; Lean and Wade, 1997; Phipps et al., 1997a; Duffels et al., 1998a; Green et al., 19991. Lower nonesterif~ed fatty acids and beta-hydroxybutyrate in blood probably reflect less body condition loss when feeding ionophores (Knowl- ton et al., 1996a; Erasmus et al., 1997; Wagner et al., 19991. The prevalence and incidence of subclinical ketosis was reduced by 50 percent when monensin was delivered by a sustained-release intraruminal device beginning at 3 weeks precalving (Duff~eld et al., 1998b). A lower incidence of bloat when feeding ionophores (Lowe et al.,1991) is proba- bly attributed to less gas production. As previously indi- cated, ionophores may have a role in the prevention of subclinical acidosis by reducing lactate formation in the rumen and stabilizing rumen pH. Direct Fed Microbials Direct fed microbials (DFM), traditionally referred to as ~~probiotics" are live or viable naturally occurring organisms supplemented to animals. Direct fed microbials have gen- erally been supplemented to animals during periods of stress or low DMI with the assumption that establishment of a beneficial microorganism population in the digestive tract will decrease or prevent pathogenic organism estab- lishment. The DFM have been fed continuously to attempt to enhance production performance, alter ruminal fermen- tation, or improve nutrient utilization. The most common DFM are fungal cultures (Aspergillus oryzae and Sacchar- omyces cerevisiae), and the lactic acid bacteria Lactobacil- Unique Aspects of Dairy CattIe Nutrition 203 lus or Streptococcus. Other bacterial species such as Bifido- bacterium spp., Bacillus spp., and Propionibacterium spp. are found in DFM, but to a lesser extent than lactic acid bacteria. Yoon and Stern (1995) in a review found that multiple modes of action have been proposed in which DFM may elicit responses, but none are clearly understood or well defined. They categorized mode of actions into the following: stimulation of desirable microbial growth in the rumen, stabilization of rumen pH, altered ruminal fermentation pattern and end prod- uct production, increased nutrient flow postruminally, increased nutrient digestibility, and alleviation of stress through enhanced immune response. Fungal Cultures Production responses to the addition of fungal cultures to diets of lactating dairy cows have been variable. Yoon and Stern (1995) reported significant increases in DMI in 2 of 10 studies and significant increases in milk production in 3 of 11 studies with supplementation of S. cerevisiae. In more recent studies, supplementation of S. cerevisiae increased DMI and milk production in three studies (Adams et al., 1995; Putman et al., 1997; Wohlt et al., 1998), but not in two others (Robinson, 1997; Kung et al., 19971. Aspergillus oryzae increased DMI in 1 of 8 studies and milk production in 6 of 14 studies summarized by Yoon and Stern (19951. In more recent studies with supple- mentation of A. oryzae to lactating cow diets, no increase in milk production was reported in one study (Bertrand and Grimes, 1997) and mixed, but an overall positive increase in milk production was reported in 46 commercial dairy herds (McGilliard and Stallings, 1998~. Stimulation of the growth and activities of both total and certain specific groups of ruminal bacteria have been the most consistent reproducible modes of action for fungal cultures (Yoon and Stern, 1995,1996; Beharka and Nagar- aja, 1998; Newbold et al., 1996~. Cellulose digesting and lactic acid utilizing bacteria are the most commonly enhanced ruminal bacteria groups by fungal supplementa- tion (Callaway and Martin, 1997~. Why and how fungal cultures increase bacterial numbers is not understood, but one proposed mechanism is that the respiratory activity of yeast protects anaerobic rumen bacteria from damage by oxygen (Newbold et al., 1996~. Dietary composition and forage source are significant factors affecting production responses to fungal cultures. High concentrate diets (60:40 concentrate to forage ratio) resulted in greater milk production response to fungal cul-

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204 Nutrient Requirements of Dairy Cattle tore supplementation than lower concentrate diets (Wil- liams et al., 1991), and ruminal digestion of NDF in alfalfa was increased more than that of NDF in corn silage or other sources of NDF by fungal culture supplementation (Miranda et al., 1996; Adams et al., 19951. Total volatile fatty acid (VFA) production or ratios of VFA are generally not affected by additions of fungal cultures (Yoon and Stern, 1995, 1996; Beharka and Nagaraja, 19981. Passage of essential amino acids or the ratio of microbial to feed nitrogen that passed to the small intestine was not increased with yeast supplementation (Putman et al., 1997) nor was overall total tract digestibility (Yoon and Stern, 19951. LACTOBACILLUS Considerably less research has been conducted to deter- mine the effects of lactic acid bacteria on production responses or ruminal fermentation changes than with fun- gal cultures. Supplementation of lactic acid bacteria to diets has primarily been for a "probiotic" effect where ingestion of beneficial organisms colonize the intestinal tract pre- venting pathogen proliferation, compete with enterotoxin- producing organisms for absorption sites in the intestine, and possibly enhance digestion of nutrients in the small intestine (Yoon and Stern, 19951. In the review by Yoon and Stern (1995), only two studies were found where Lacto- bacillus acidophilus was fed to lactating dairy cattle. In both studies, milk production increased by feeding L. acid- ophilus. Cruywagen et al. (1996) reported supplementing L. acidophilus in milk replacer resulted in calves losing less weight the initial two weeks of life, but over a six-week period had no affect on weight gain, feed intake, or diarrhea occurrence. The addition of L. acidophilus or Bifidobacter- ium animalis to a milk replacer containing an antibiotic increased growth rate and efficiency of feed utilization by calves during the milk replacer feeding period (first 35 days of life) and the next 21 days postweaning (Abe et al., 19951. Bovine Somatotropin Bovine somatotropin (BST) is a naturally-occurring pro- tein hormone produced in the pituitary gland of dairy cattle. It is a major regulator of growth and milk production. This hormone can be produced in commercial quantity using recombinant DNA technology. BST was approved for use in lactating dairy cows by the Food and Drug Administration in November 1993. Because of a 90-day moratorium passed by the U.S. Congress, BST could not be sold for commercial use until February 1994. Supplementation of BST to growing and lactating ani- mals affects many physiologic processes (Peel and Bauman, 1987; Bauman et al., 1989a; National Research Council, 19941. Metabolic adaptations that partition increased quan- tities of absorbed nutrients to the required tissue for opti- mum growth or milk production is the principle effect of BST in growing and lactating dairy cattle. Supplementation of BST to growing or lactating dairy cattle does not affect digestibilities of DM, energy, or protein (Bauman et al., 1989a; Boyd and Bauman, 1989; Chalupa and Galligan, 1989) nor does BST affect energy utilization for mainte- nance or the partial efficiency of milk synthesis (Tyrrell et al., 1988; Sechen et al., 1989; Kirchgessner et al., 19911. However, the efficiency of overall nutrient utilization for milk production by cows is improved because a smaller proportion of the nutrient intake is needed to fulfill the maintenance requirements. The effects of BST on milk yield have been reviewed (Peel and Bauman, 1987; Chilliard, 1989; McBride et al., 1988; Chalupa and Galligan, 1989; Peel et al., 1989; Crooker and Otterby, 1991; Hartnell et al.,1991; McGuffey and Williamson, 1991; Bauman, 1992; National Research Council, 1994; Bauman et al., 19991. Increases in milk yield to varying doses of BST (5 to 50 mg/cow/day) range from about 3 to 6 kg of milklcow/day (National Research Council, 19941. Persistency of lactation also is improved. Supplementation of BST has increased milk yield in all breeds of dairy cattle studied and in animals of different parity and genetic potential (National Research Council, 19941. The magnitude of the increased milk yield will be affected by the quality of management, especially nutrition management (Bauman, 19871. Nutritional status, diet composition, environment, sea- son, stage of lactation, genetics, and age affect the concen- tration of fat and protein in milk (Linn, 1988; Sutton, 19891. These factors also affect the composition of milk from cows supplemented with BST. The nutritional status of cows both before and during supplementation of BST deter- mines the effect of BST on the concentration of fat and protein in milk (Peel and Bauman, 1987; McBride et al., 1988; Bauman et al., 1989a; Chalupa and Galligan, 1989; van den Berg, 1991; Dell'Orto and Savoini, 1991; Barbano et al., 1992; Lynch et al., 1992; Laurent et al., 19921. Short- term changes in milk composition when BST is supple- mented may occur because of increased milk synthesis and because of increased mobilization of energy and protein from body reserves to meet the increased nutrient demands for synthesis of milk and milk components. However, when BST was supplemented for a complete lactation the con- centration of fat and protein in milk was not different for control and BST cows (Bauman et al., 1989b). BST did not affect milk composition during long-term supplementa- tion, because cows, within a few weeks after the start of BST administration, increased nutrient intake to meet requirements for synthesis of milk and milk components and to replenish body reserves (Peel and Bauman, 1987; Chalupa and Galligan, 1989; Chilliard, 19891. High quality feeds and excellent nutrition management are required to

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attain maximum response from cows supplemented with BST (Bauman, 1987, 19921. Nutrition of daily cows supplemented with BST has been discussed in several papers (Bauman, 1987; Chalupa and Galligan, 1989; Chilliard, 1989; Crooker and Otterby, 1991; Kirchgessner et al., 1991; McGuffey and Wilkinson, 1991; Muller, 1992; Collier et al., 1992; National Research Council, 19941. Nutrient requirements are identical for BST supplemented cows and unsupplemented cows if they are producing the same amount of milk with an identical composition, have the same body size and weight, and are losing or gaining the same body weight. Diet formulation and feeding strategies should be the same for BST supple- mented and unsupplemented cows of the same size and weight that are producing the same amount of milk and milk components. Current recommendations are that cows supplemented with BST should be fed and managed like unsupplemented cows at similar levels of production. REFERENCES Abe, F., N. 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