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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
OCR for page 185
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 pregnant—280. 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-
OCR for page 186
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 - 0.69e°35t (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
OCR for page 187
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-
OCR for page 188
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
OCR for page 189
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
OCR for page 190
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
OCR for page 191
- - ~
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-
OCR for page 192
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
OCR for page 193
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
OCR for page 194
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.,
OCR for page 203
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-
OCR for page 204
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
OCR for page 205
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.
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Representative terms from entire chapter:
milk fat
