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Transcript of 2013 South West Nutrition Proceeding
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Proceedings of the
28th
Annual
Southwest Nutrition
and
Management Conference
Tempe, Arizona
February 21 & 22, 2013
Sponsored by:
The University of Arizona
Department of Animal Sciences
Coordinating Committee
Moe Bakke Jerry Kennedy Fred Owens
Lance Baumgard Jim Loughead John Smith
Robert Collier Rick Lundquist Lawson Spicer
Ken Eng Chel Moore Matthew VanBaale
Mitch Etchebarne Naji Nassereddine Ueli Zaugg
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ii
28th
Annual
Southwest Nutrition and Management Conference
CONFERENCE SPONSOR
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28th
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Zook Nutrition and Management
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28th
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SILVER SPONSORS Adisseo Maid Rite Feeds QualiTech
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ix
Table of Contents
Prince Agri Products, Inc. - Pre-Conference Symposium
DCAD Revisted: Prepartum Use to Optimize Health and Lactational Performance David Beede, Ph.D.
Michigan State University…………………………………………….………………….1
Mastitis and Dairy Replacement Heifers: Management Practices to Reduce the Odds Stephen Nickerson, Ph.D.
University of Georgia ……….………...…..…………………………………………….19
The Physiology of Stress and Effects on Immune Health in Ruminants Jeff Carroll, Ph.D.
USDA/ARS………………..………...…...………………………………………………..35
Predicting Transition Cow Health and Performance – Use of Blood and Fecal Biomarkers
for Herd-Level Evaluation and Diagnostics Thomas Overton, Ph.D.,
Cornell University……………………………………………………………………..45
Southwest Nutrition and Management Conference
Economics of Feeds in Dairy Rations Normand St. Pierre, Ph.D.
Ohio State University…………………………………………………...…..………….57
Managing Heat Stress and its Impact on Cow Behavior John Smith, Ph.D.
University of Arizona…………………………………………………………………….68
Early Weaning Beef Calves to Improve Herd Productivity: Implications on Cow and Calf
Nutrition John Arthington, Ph.D.
University of Florida………...…………………………………………………………80
BH in the Rumen: The Gateway to Seeing Benefits from Fat Supplements Thomas Jenkins, Ph.D.
Clemson University……………………………………………………………………..94
Why Cows Die on Dairies Franklyn Garry, Ph.D.
Colorado State University…….………………………..………………………..……110
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x
An Update on Hypocalcemia on Dairy Farms
Garrett Oetzel, Ph.D.
University of Wisconsin-Madison….…………………………………………………117
Performance of Calves in Different Calf Feeding Systems Mark Hill, Ph.D.
Provimi Nutrition………………...………………………………………………......128
Update on Milk Fat and Human Health Adam Lock, Ph.D.
Cornell University…………………………………………………………………….141
Use of Probiotics in Dairy Rations During Heat Stress Laun W. Hall
University of Arizona……………………………………………………...………….153
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1
DCAD Revisited: Prepartum Use to Optimize Health and Lactational
Performance
J. A. Shire and D. K. Beede
Department of Animal Science
Michigan State University
Corresponding author: [email protected]
SUMMARY
Normal calcium (Ca) status is extremely important through the transition period to launch a
healthy and successful lactation.
From recent evidence, routine monitoring to identify subclinical hypocalcemia (defined by
early postpartum blood serum Ca of less than 8.6 mg/dl) would be appropriate in herds with
unacceptable periparturient health disorders.
Based on available analyses the four-element equation for dietary cation-anion difference
[DCAD = (Na+ + K
+) – (Cl
- + S
2-)] is most appropriate to formulate a reduced DCAD of the
close-up ration.
The most effective first step to lower the DCAD is to reduce K+ and Na
+ as much as
possible before supplementing anions.
DCAD of -10 mEq/100 g is recommended; a somewhat lower DCAD (-15 mEq/100 g) may
be advantageous to help accommodate biological variation among animals within the close-
up group.
Close-up diets with 1.0% Ca and 0.35% Mg are sufficient in properly supplemented anionic
diets to support normal periparturient Ca status.
Various vitamin D-related processes, including regulation of periparturient Ca status, might
be improved with supplementation of vitamin D throughout the close-up period.
The body of evidence accumulated over the last 40+ years highlights the direct and indirect
importance of periparturient Ca status and how Ca status can be improved by manipulation
of close-up DCAD to improve lactational performance.
Future research should consider: a) timing of vitamin D supplementation prior to calving; b)
factors that contribute to vitamin D receptor regulation in the transition period; and, c)
performance of heifers fed anionic diets.
INTRODUCTION
The importance of successfully transitioning dairy cows from pregnancy to lactation has been
known for decades. Periparturient hypocalcemia can be detrimental to both cows and dairy
producers. If preventive measures to manage blood calcium (Ca) around parturition are not
taken, a cascade of metabolic problems can lead to secondary health issues, impaired immune
function, reduced milk production, and poor reproductive performance. Elliot Block (1984) was
first in North America to report that reducing the dietary cation-anion difference (DCAD) before
calving could benefit early postpartum Ca status and aid transition into lactation. In the late
1980s and early 1990s the so-called “anionic salts” were supplemented in close-up diets.
Success was variable mainly because of lack of understanding about how to deliver this new
technology. Often prepartum feed intake was reduced with the salts. Consequently, commercial
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anion supplements apparently causing fewer feed intake problems became available.
Nonetheless, anion supplementation still does not work as well as desired in some cases. This
paper takes a brief look back at the development of the DCAD strategy for transition dairy
cows, suggests some possible reasons why it is not more universally efficacious, and addresses
current approaches to monitor and reduce risk of hypocalcemia as well as new ideas to consider
when implementing the prepartum DCAD strategy.
HYPOCALCEMIA
Subclinical Hypocalcemia
Hypocalcemia is a critical concern due to the enormous physiological demands for Ca at calving
and the start of lactation (Oetzel et al., 1988; Horst et al., 1997). Calcium demand of a cow at
initiation of lactation is about double compared with when she was non-lactating and pregnant.
For example, the Ca requirement of a 1600-pound pregnant dry cow increases from about 11 g/d
to support the conceptus to about 23 g/d after calving to support milk production (Goff and
Horst, 1997a). In order to suffice, a cow must bring at least 30 g of Ca/d into the plasma pool in
very short order by intestinal absorption and(or) bone resorption (Horst et al., 1997). This is a
formidable physiological task.
Normal blood plasma Ca concentration is tightly regulated and generally kept between 8.5 to 10
mg/dl (2.1 to 2.5 mM; Cahn and Line, 2005). In the periparturient period with enormous
physiological demands, blood Ca may drop below this range; though is not characteristically
considered subclinical until blood plasma Ca drops to the range of 8.0 to 5.5 mg/dl (2.00 to 1.38
mM), but with homeostasis still maintained (Goff, 2008). Recent findings suggest that the
subclinical range might be widened to include blood serum Ca concentrations of 8.6 to 5.5
mg/dl to better identify cows at risk for metritis (Martinez et al., 2012). The point at which a
cow is truly hypocalcemic and biological functions become impaired varies among individual
cows; their “capacity” to maintain homeostasis and Ca status as influenced by several factors is
discussed subsequently. A possible on-farm strategy might be to more routinely monitor and
identify subclinical hypocalcemia as serum Ca concentrations of less than 8.6 mg/dl in herds
with unacceptable incidences of periparturient health disorders.
Clinical Hypocalcemia
Milk fever (clinical hypocalcemia) defines an extreme decrease in blood plasma Ca below a
certain point around time of calving resulting in homeostatic failure. The point at which it is
considered clinical was suggested to be below 5.5 mg/dl (Goff, 2008). Milk fever may or may
not be accompanied by other signs such as poor appetite, recumbency, and lethargy (Horst et al.,
1997). A study conducted by the USDA National Animal Health Monitoring System (2002)
estimated a 5% incidence rate of milk fever in the United States (Reinhardt et al., 2011). Failure
to maintain muscle tone and contractility of the gastrointestinal tract and the cardiovascular
system quickly leads to death in the majority of milk fever cases (Cahn and Line, 2005). Not all
cows that have subclinical hypocalcemia develop milk fever, but it is important that diagnostic
and preventive measures are taken before the cow’s health declines and subsequent problems
arise.
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Predisposing Factors
Reasons for susceptibility to hypocalcemia vary and may be multi-factorial. One of the most
commonly noted differences in susceptibility is parity. Incidence of subclinical hypocalcemia
(< 8.0 mg plasma Ca /dl) typically rises with increasing parity, affecting 25% of heifers and
almost half of cows of second and greater parity (Reinhardt et al., 2011). It is thought that
heifers especially are less susceptible because they have greater bone depletion/repletion activity
and are more able to mobilize bone Ca from their Ca reserves than are later parity cows (van
Mosel et al., 1993). Additionally, later parity cows produce more colostrum and milk making
the demand for Ca greater. A similar relationship with parity was noted with clinical milk fever
affecting less than 1% of heifers, but surpassing 6% for cows of third and greater parity
(Reinhardt et al., 2011). This greater milk fever risk and incidence is in part due to parity as
well as history of previous milk fever. History of milk fever seems to be a large determinant of
whether or not a cow develops hypocalcemia and milk fever at subsequent parturitions. This is
presumably due to a decreased ability of these particular cows to respond immediately to
biological signals and increase vitamin D receptor (VDR) numbers in a timely manner (Goff et
al., 1995a). Blood Ca and vitamin D3 concentrations are obviously important components in Ca
mobilization, bone resorption, and intestinal absorption (Jones, 2008). However, deficiencies in
dietary Ca, vitamin D, or biologically active 1, 25 dihydroxyvitamin D are not thought to be the
casual reasons for hypocalcemia. For instance, low Ca diets were used successfully to reduce
incidence of hypocalcemia (Goings et al., 1974; Thilsing-Hansen et al., 2002) and active
vitamin D plasma concentrations usually are considered sufficient in afflicted cows (Goff et al.,
1989). A possible explanation for the metabolic cause of hypocalcemia is slow VDR up-
regulation, and(or) overall lower VDR numbers between breeds (e.g., Jersey vs. Holstein; Goff
et al., 1995b). Jerseys have fewer overall VDR compared with Holsteins (Goff et al., 1995b)
and Jerseys are more susceptible to milk fever (Lean et al., 2006). Conversely, Holsteins have
similar numbers of receptors compared with Brown Swiss (Lisegang et al., 2008) and both
breeds typically have less incidence of milk fever than Jerseys. The regulation of VDR could be
a very plausible explanation for differences among breeds and whether or not a particular cow
of a particular parity or breed develops hypocalcemia and to what severity the disorder
manifests.
DIETARY CATION-ANION DIFFERENCE
History and Current Use
The ability to reduce the incidence of periparturient hypocalcemia through addition of mineral
acids to the diet was first documented by Ender and Dishington (1970). Shortly thereafter they
showed that multiple dietary anionic salts were effective in stimulating increased blood Ca
(Ender et al., 1971; Dishington, 1975). Block (1984) introduced the dietary cation-anion
balance theory to transition cow research in North America. He demonstrated that providing
more dietary fixed anions than cations via anionic salts in the close-up period increased blood
Ca in early postpartum cows. Today, this strategy is commonly known as dietary cation-anion
difference (DCAD), which more specifically addresses the calculation of DCAD in ration
formulation (Sanchez and Beede, 1991).
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The DCAD can be calculated as several variants of an equation involving more or less of the
seven dietary essential macromineral elements: milliequivalents (mEq) of [(Na+ + K
+ + Mg
++
Ca2+
) - (Cl- + S
2- + P
3-)/100g of dietary DM]. As part of a ration formulation and management
strategy, a low or negative DCAD is supplied in the diet for 2 to 3 wk prepartum (Block, 1984;
Oetzel et al., 1988). An effective DCAD reduction changes the acid-base status of the cow
within 36 hr (Goff and Horst, 1998). However, because of variation in actual compared with
expected calving day (e.g., 8 to10 d, S.D.) sufficient time of dietary provision must be used to
accommodate the majority of cows in the close-up group. Anion supplementation effectively
reduces the incidence of periparturient hypocalcemia and milk fever by increasing the
concentration of blood Ca (Block, 1984; Oetzel et al., 1988). Early on, the so-called anionic
salts (e.g., chloride and sulfate salts of ammonium, calcium or magnesium) were used. Certain
anionic salts were thought to be more palatable than others (e.g., greater DMI when magnesium
sulfate compared with calcium chloride was supplemented; Oetzel and Barmore, 1993). In the
USDA survey, an estimated 27% of U.S. dairy operations used “anionic salts” (as specifically
worded in the survey) to decrease DCAD in an effort to reduce incidence of periparturient
hypocalcemia (USDA, 2007). Use of commercial products to supplement anions rather than
anionic salts is much more popular today than in the past due to their ease of use and often the
added benefit as a source of protein. The use of palatable carriers and addition of flavoring in
commercial sources may help dilute or mask the presumably bitter taste thought to accompany
pure anionic salt sources. The first-line, most efficacious strategy for lowering DCAD is to
reduce the strong cations (i.e., K+ and Na
+) before adding anion sources. About 47% of U.S.
dairy operations specifically aimed to lower dietary K in efforts to reduce DCAD of prepartum
diets (USDA, 2007).
DCAD Equations
There are a variety of ways to calculate DCAD depending on which macromineral elements
(fixed ions) are considered important (Ender et al., 1971; Goff, 2004). Most equations include
Na, K, Cl, and S, but variations on this come from addition of Ca and Mg, estimated coefficients
of absorption for the different mineral elements, and the inclusion or exclusion of S and P.
Overall, the most widely used equation in the industry is that originally used by Ender et al.
(1971) [DCAD = (Na+ + K
+) – (Cl
- + S
2-)]. Based solely on the acidifying effect of dietary S in
urine and blood, Spanghero (2004) suggested that S had negligible influence on the cow’s acid-
base balance in the basic four-element equation. Thus, the simpler three-element equation
[DCAD = (Na+ + K
+) – (Cl
-)] was suggested. However, increased S in the diet was associated
with decreased incidence of milk fever and the source of S (as part of an organic compound or
as supplemental sulfates) could be a factor (Lean et al., 2006). Note that supplementation of
elemental sulfur (e.g., the flowers of sulfur) is worthless as it does not provide absorbable S nor
does it have acidifying properties as part of the DCAD calculation.
The meta-analysis of Lean et al. (2006) assessed the ability of four relevant DCAD equations to
both affect acid-base status and to predict milk fever of Holstein, Norwegian and Swedish Red
and White, and Jersey cows. It is important to note that using an equation to predict the effects
of macromineral elements on milk fever is not necessarily the same as using an equation to
predict overall acid-base status. For example, Jerseys have a greater susceptibility to milk fever
than Holsteins (Lean et al., 2006), while Mg inclusion in the diet reduced risk of milk fever but
made the DCAD value more positive. A criterion for data inclusion in the study of Lean et al.
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5
(2006) was that they could calculate DCAD from information given in the original reports;
however, lactation number, which is a recognized risk factor for milk fever (Reinhardt et al.,
2011) was not in the model. The analysis also did not consider Ca in the DCAD equation noting
that diets with both low Ca (0.5 %) and high Ca (> 1.0 %) were effective in preventing milk
fever. Additionally, in their analysis there was a time by treatment interaction on the efficacy of
Ca inclusion rate and lack of sufficient data with dietary Ca inclusion greater than 1.1%.
Results indicate that [DCAD = (Na+ + K
+) – (Cl
- + S
2-)] was the most effective in describing
acid-base status as well as predicting reduced incidence of milk fever. Similarly, a meta-
analysis by Charbonneau et al. (2006) concluded that [DCAD = (Na+ + K
+) – (Cl
- + 0.6S
2-)]
correlated with milk fever incidence and acid-base status prediction. The 0.6 coefficient was
based on findings of Tucker et al. (1991a) and later supported by Goff et al. (2004) indicating
that S had less acidifying effect compared with Cl. Diet composition and desired outcome (i.e.,
risk prevention or acidifying ability) should be important considerations when determining
which equation to use. Based on all of the available information the four-element equation
seems most acceptable. Whether or not the 0.6 coefficient for S should be incorporated likely
depends upon the sources of supplemental S in a particular diet.
Mechanism of Action
Metabolic acidosis or alkalosis results from the change in electrical charge of biological fluids
due to either more anions (i.e., acidosis) or more cations (i.e., alkalosis) entering the blood. The
change in electrical charge of the blood results in transfer of H+ ions and changes in blood pH
(i.e., acid-base balance; Goff, 2008). Blood pH is tightly regulated within a narrow normal
physiological range, keeping arterial blood pH between 7.35 to 7.45 and venous blood at a
slightly lower pH (Nagy et al., 2001). Though blood pH can be reduced through use of negative
DCAD, these changes may not be significant (Charbonneau et al., 2006; Grünberg et al., 2011).
A meta-analysis indicated a significant negative relationship between decreasing DCAD (from
+30 to 0 mEq/100g) and decreasing blood pH; however, the change in blood pH was very small
and not statistically significant (Charbonneau et al., 2006). Compared with sulfate salts, chloride
anionic salts are thought to have a greater acidifying effect in blood (Goff et al., 2004;
Charbonneau et al., 2006).
A more easily accessible proxy for monitoring systemic acid-base status in the field is urine pH.
Typically if urine pH is below 7.0 then systemic acidosis has been generated (Jardon, 1995).
Charbonneau et al. (2006) suggested that inducing acidosis beyond the point where urine pH
drops below 6.8 is not warranted in field application of the DCAD strategy because risk of
hypocalcemia was not further reduced. Typical anionic salts fed in close-up rations with
negative DCAD include chloride and sulfate salts of calcium, magnesium, and ammonium.
Hydrochloric acid was most effective at lowering urine pH compared with the anionic salts
(Goff et al., 2004).
The exact mechanism by which a low or negative DCAD aids in the reduction of hypocalcemia
during the periparturient period is not completely understood. It apparently has to do with two
independent mechanisms. First, the mildly acidic systemic environment created by lowered
DCAD stimulates osteoclasts to start mineralizing bone Ca to correct the acidosis. Under
hypocalcemic conditions parathyroid hormone (PTH) is secreted. This hormone assists in the
subsequent formation of the active 1, 25 dihdroxyvitamin D hormone (1,25 [OH]2 D). Through
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both PTH and biologically active vitamin D, bone resorption of Ca is stimulated (Horst and
Reinhardt, 1983). Additionally, there is increased renal tubular resorption of Ca and increased
efficiency of Ca absorption in the small intestine (Goff and Horst, 2003). Together these
mechanisms and newly available Ca sources contribute to the return of Ca homeostasis.
Further connection between anion supplementation and Ca status is thought to be due to the
decrease in blood pH by anions (Goff, 2008). When both pH is low and PTH is active,
osteoclastic activity is even greater and thus Ca resorption increases significantly (Bushinsky,
2001). It is commonly accepted that the reason for this increased activity is that the creation of
an acidic metabolic environment allows increased tissue responsiveness to PTH. When blood
pH is more alkaline (>7.35), PTH cannot tightly bind to its receptors on the bone surface and in
renal tissue. However, when blood is at its normal physiological pH of 7.35, PTH is tightly
bound to its receptors and can therefore better stimulate its target cells (Bushinsky, 2001; Goff,
2008).
“Optimal” DCAD for Close-up Cows
It is not necessary for the prepartum DCAD to be negative in order to stimulate homeostatic
acid-base mechanisms and increase blood Ca. Lowering DCAD from +30 to 0 mEq/100g
resulted in a decrease of urine pH from a normal of 8.09 to 7.01 (Charbonneau et al., 2006).
Furthermore, this mild systemic acidosis resulted in significant increase (~11%) in total blood
Ca concentration immediately postpartum and reduced incidence of milk fever from 16.4 to
3.2%. In another study, cows fed close-up diets with a negative DCAD (-10 to -12 mEq/100 g)
with supplemental calcium chloride and calcium sulfate (personal communication with authors)
or a commercial supplement did not have increased blood Ca after calving compared with cows
fed a control ration (+22 mEq/100g) (DeGroot et al., 2012).
It was suggested that systemic acidic conditions decrease the ability of insulin to bind to its
receptor (Whittaker et al., 1982). This causes reduced insulin sensitivity resulting in decreased
glucose uptake and utilization (Bigner et al., 1996). Because of the shift in energy demand at
onset of lactation, loss of utilizable glucose can be detrimental to both milk production and cow
health. Grünberg et al. (2011) did not observe an effect on insulin response or sensitivity when
mild systemic acidosis was induced through use of anion supplementation (-9 mEq/100 g).
Similarly, Ramos-Nieves et al. (2009) and DeGroot et al. (2010) found no difference in plasma
glucose concentrations during the periparturient period in relation to DCAD prepartum (-15
mEq/100 g and -12 mEq/100 g, respectively).
The influence of anion supplementation on DMI varies among studies. Both Block (1984) and
Oetzel et al. (1988) found no changes in prepartum DMI when anion sources were provided (-13
mEq/100 g and -7.6 mEq/100 g, respectively). DeGroot et al. (2010) also observed changed
acid-base status without compromising prepartum DMI in multiparous cows, but observed
increased postpartum DMI (2.1 kg/cow per d) for cows receiving anion supplementation
prepartum. These findings differ from a meta-analysis that indicated a decrease in prepartum
DMI of 1.3 kg/cow per d when DCAD was reduced from +30 to 0 mEq/100g (Charbonneau et
al., 2006). Ramos-Nieves et al. (2009) also reported a significant decrease in DMI (15.6 vs.
14.4 kg/cow per d) when prepartum anion supplementation was provided (+10 vs. -15 mEq/100,
respectively). This discrepancy could be due to the amount and(or) source of anions
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7
supplemented to reach a desired DCAD. Sodium and K are recognized as strong cation
contributors with greater dietary concentrations being linked to increased incidence of milk
fever (Goff and Horst, 1997b; Lean et al., 2006). For most effective DCAD formulation, dietary
Na and K should be reduced as much as practically possible before adding supplemental anions.
In order to avoid possible adverse effects of supplemental anions on DMI while still achieving
mild systemic acidosis, a DCAD of -10 mEq/100 g is suggested. Using a somewhat lower
DCAD (e.g., -15 mEq/100 g) may be advantageous to help accommodate biological variation
among individual cows (i.e., fluctuations in daily DMI and differences in biological ability to
maintain acid-base balance).
Management of Heifers (Primiparous Cows)
Although primiparous cows do not typically experience as many or the severity of Ca-related
metabolic problems during transition as multiparous cows, both pregnant heifers and
multiparous cows are often in the same group and fed the same close-up ration. The USDA
(2007) survey suggested that about 20% of dairy farms use anion supplementation in close-up
rations for heifers. A possible adverse effect of providing a negative DCAD to heifers is
reduced DMI (Tucker et al., 1991b; Moore et al., 2000); but, other negative effects are largely
not reported. DeGroot et al. (2010) demonstrated that using various anion sources (commercial
supplements, or calcium sulfate and calcium chloride) to create a negative DCAD during the
close-up period did not result in any obvious negative side effects in pregnant heifers. Acid-
base balance was effectively altered with heifers having lower prepartum urine pH compared
with multiparous cows (6.24 and 6.80 respectively). Similar to the multiparous cows, the
prepartum DMI of heifers was not impacted and early postpartum DMI increased (1.4 kg/cow
per d). Overall, there is insufficient evidence to say whether or not heifers/primiparous cows
will be impacted negatively in major ways if provided a negative DCAD diet in late gestation.
The lowered prepartum urine pH (i.e., affected acid-base status) of heifers could be an
unnecessary consequence considering there was no significant change in postpartum plasma Ca
concentrations. Overall management of heifers must still be considered when deciding on anion
supplementation. Improper monitoring of mixed parity close-up groups may lead to
competition among animals and reduced DMI of typically smaller heifers.
DCAD and Milk Yield Response
Prepartum anion supplementation improved lactation performance in some studies. Block
(1984) reported a 6.8% increase in milk yield of cows given anionic salts (DCAD: -13 mEq/100
g) in the close-up period with no reported change in postpartum DMI. Likewise, high producing
multiparous cows provided diets supplemented with anions (-10 to – 12 mEq/100 g) prepartum
increased milk yield by 18% (6.5 kg/cow per d) compared with cows fed a control diet (+22
mEq/100 g; DeGroot et al., 2010). This increase was likely due to greater DMI of cows fed
anions prepartum. Differences in milk yield are not always found. No changes in milk yield,
milk composition, or postpartum DMI were found when comparing prepartum anionic vs.
cationic diets (-15 vs. +15 mEq/100g by Moore et al., 2000; or, -15 vs. + 10 mEq/100g by
Ramos-Nieves et al., 2009). Similarly, milk yield and postpartum DMI did not differ among
cows in a pasture system provided a prepartum diet with a DCAD of +50 vs. +7 mEq/100g
(Roche et al., 2003). The improvement in some studies from feeding a low or negative DCAD
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prepartum on postpartum milk yield is most likely due to improved periparturient Ca status and
health, and improved postpartum DMI.
MACROMINERALS
Cations
Whether or not feeding less or more dietary Ca than the cows’ requirement in close-up diets is
still questioned. To truly restrict Ca intake below requirement to affect Ca homeostasis, less
than 20 g/cow per d is required (Thilsing-Hansen et al., 2002) or possibly less than 15 g/cow per
d (Goings et al., 1974). The current NRC (2001) recommendation for absorbed Ca for a
pregnant Holstein dry cow (1600 lb BW) is approximately 11 g/d (or about 20 - 30 g of total
dietary Ca/cow per d). By markedly restricting dietary Ca prepartum, hypocalcemic-like
conditions are induced prior to calving. This results in increased fractional absorption of Ca
from the small intestine, renal reabsorption, and bone resorption (Goff and Horst, 2003).
Because these mechanisms are stimulated before calving, increased Ca in blood at calving can
result (Goings et al., 1974; Thilsing-Hansen et al., 2002).
The relatively high Ca content of some forages and byproduct feeds can make dietary restriction
of Ca difficult. Furthermore, the concentration of Ca in the diet is not as important a factor in
occurrence of milk fever as other macromineral cations such as K, Na and Mg (Goff and Horst,
1997b; Lean et al., 2006). Whether or not there is an interaction between DCAD and Ca has
been questioned (Goff and Horst, 1997b; Oba et al., 2011; Goff and Horst, 2012). In a classic
study, Goff and Horst (1997b) were the first to directly assess the effects of increasing dietary
Ca and K (that is increasing DCAD) on hypocalcemia. They found no change in incidence of
milk fever of multiparous Jersey cows with 0.5% vs. 1.5% Ca in the close-up diet. However,
hypocalcemia increased when greater concentrations of Na and K were incorporated into the
diet regardless of Ca concentration. This response demonstrated clearly that the overall effect of
DCAD, independent of dietary Ca, greatly influenced occurrence of hypocalcemia. The more
influential effect of Na and K compared with Ca on incidence of milk fever was later confirmed
by meta-analysis (Lean et al., 2006). They also observed increased milk fever when close-up
diets had greater Ca (0.5 vs. 1.0%). An even more significant increase in milk fever was
observed when cows were fed close-up diets with >1.5% Ca. In their study, length of time of
feeding high Ca diets and few data with high Ca close-up diets may be contributing factors
explaining why dietary Ca did not affect incidence of milk fever. Higher dietary Ca might be
beneficial if fed longer than 20 d (Lean et al., 2006), though a 14-d period was a long enough to
show a beneficial effect of high Ca in another study (Oba et al., 2011). From these studies it
appears that a Ca inclusion rate of 1.0% in close-up diets is sufficient to maintain periparturient
blood Ca provided that an anionic diet is fed.
Calcium and DCAD
The aforementioned difference in response to DCAD rather than dietary Ca could be explained
in a couple of ways. Limiting Ca in a positive DCAD diet causes some degree of hypocalcemia
and stimulates PTH to increase blood Ca before calving (Thilsing-Hansen et al., 2002). On the
other hand, the mild metabolic acidosis that results from a negative DCAD increases
hypercalciurea (Vagnoni and Oetzel, 1998). Thus, feeding greater Ca with anion
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supplementation could aid in maintaining blood Ca concentrations around calving. Oba et al.
(2011) examined both of these concepts by supplementing diets with moderate or low Ca (0.9%
vs. 0.3%) with DCAD of -6.4 or +9.1 mEq/100 g and challenging cows with intravenous EDTA
(a blood Ca-chelator) infusion. The time for cows to recover to 90% of their pre-challenge
blood ionized-Ca concentration was shorter for those fed +9.1 mEq/100 g DCAD with 0.3%
dietary Ca and for those fed -6.4 mEq/100 g DCAD with 0.9% Ca; whereas, the time for cows
to reach their pre-challenged ionized-Ca status was longer for those fed +9.1 mEq/100 g DCAD
with 0.9% Ca as well as those fed the -6.4 mEq/100 g DCAD with 0.3% Ca. A significant
interaction of dietary Ca% by DCAD on time to recover to 90% of pre-challenge ionized blood
Ca also was detected. Conversely, Goff and Horst (2012) found no advantage in the cows’
ability to increase blood Ca when fed 1.5% Ca compared with 0.5% Ca while on negative
DCAD diets (-6.1 and -6.8 mEq/100 g). Also, Chan et al. (2006) noted no change in blood Ca
with anion supplementation (-6 mEq/100 g) and either moderate (0.99%) or high (1.5%) dietary
Ca. These findings support the idea that the DCAD in the close-up diet is much more influential
on development of hypocalcemia than dietary Ca concentration per se. Perhaps the differences
in recovery time of blood ionized-Ca in response to DCAD with varying dietary Ca found by
Oba et al. (2011) was actually due to differences in DCAD. Theoretically, the treatment group
(+9.1 mEq/100 g with 0.9% Ca) that had the greatest recovery time also would have the greatest
DCAD value due to increased Ca inclusion.
Calcium Status and Milk Yield
Besides troublesome health effects associated with periparturient hypocalcemia (Curtis et al.,
1983), lactation performance can be impacted by Ca status in early lactation. Kimya et al.
(2005) reported increased milk production of both primiparous and multiparous cows (1.7 and
3.9 kg/cow per d, respectively) when blood Ca status was maintained on a low Ca diet (0.46%).
Additionally, milk Ca, P, and Mg were not affected by changes in close-up Ca concentration
(0.46% vs. 0.86%) for any parity. In another study where normal blood Ca was maintained
around parturition and moderate or high Ca was fed prepartum (0.99% vs. 1.5%) there was no
difference in milk yield or composition (Chan et al., 2006). Interestingly, Jawor et al. (2012)
reported increased milk yield of hypocalcemic cows during the first few weeks of lactation. The
biggest difference was in third lactation cows where milk yield remained greater for
hypocalcemic compared with normocalcemic cows through 280 DIM before declining.
However, other researchers observed no differences in the milk yield of hypocalcemic compared
with normocalcemic cows (Martinez et al., 2012). In another study, milk yield was reduced by
hypocalcemia (-3.2 kg of milk/cow per d; Chapinal et al., 2012). These differences in
lactational performance among various studies demonstrate the importance of proactive
approaches for monitoring and treating hypocalcemia.
Magnesium and Calcium
Magnesium is extremely important in homeostatic mechanisms to correct hypocalcemia.
Magnesium deficiency impairs PTH secretion and PTH receptor response resulting in blunted
Ca mobilization and hypocalcemia (Johannsson and Raisz, 1983); thus, exacerbating and
predisposing hypocalcemic conditions around parturition. Cows that do not maintain
normocalcemia around parturition had reduced blood Mg concentrations as well (Martinez et al.,
2012). Normal plasma Mg concentration is 1.8 to 2.4 mg/dl (0.75 mM to 1.0 mM; Goff, 2008).
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Whereas, Mg did not have a strong influence on predicting acid-base response to varying
DCAD (Charbonneau et al., 2006; Lean et al., 2006) dietary Mg concentration is thought to
influence occurrence of milk fever. An increase in dietary Mg concentration (0.3 to 0.4%)
greatly reduced milk fever incidence (Lean et al., 2006). The recommended concentration of
dietary Mg is 0.35 to 0.40% (Goff, 2008).
An interaction between high dietary Ca and Mg absorption may exist. Close-up cows fed 1.36%
Ca and 0.18% Mg had lower apparent Mg digestibility and urinary Mg excretion compared with
cows provided 0.45 or 0.90% Ca (Kronqvist et al., 2011). It should be noted that prepartum
DCAD was positive (~20 mEq/100g); based on urinary Mg excretion all cows in this study were
subclinically hypomagnesmic. In another study, blood Mg was not changed when 55 to 91 g of
Ca/cow per d (0.46 to 0.86% Ca) were provided with 0.18% dietary Mg (Kamiya et al., 2005).
In that study the DCAD was not reported and there was no increase in blood PTH or bone
resorption markers.
VITAMIN D
Vitamin D Activation and Receptor Regulation
Vitamin D metabolites such as 1,25 (OH)2 D3 have a variety of important physiological roles
such as cellular differentiation, Ca signaling (Jones, 2008), and immunological functions
(Kimura et al., 2006; Nelson et al., 2010). Failure of these biological functions due to vitamin D
deficiency can exacerbate and complicate the effects of hypocalcemia. As a result, risk of
secondary health problems such as mastitis, displaced abomasum (Goff, 2008), and poor
reproductive performance (Ward et al., 1970) are increased greatly.
Vitamin D is needed when plasma Ca drops below its homeostatic range. Through Ca and PTH
signaling the vitamin (hormone) is released from its stores and transported to the liver via
binding proteins (Jones, 2008). In the liver vitamin D is hydroxylated, forming 25
hydroxyvitamin D (25OHD). This newly formed vitamin D metabolite is then transported
through blood to the kidney where it is fully activated by another hydroxylase and converted to
the active form 1,25 (OH)2 D (Jones, 2008).
The role of active vitamin D in intestinal Ca absorption is crucial (Goff and Horst, 2003; Jones,
2008). There are a couple of theories as to how vitamin D status might influence hypocalcemia.
Questioned initially was whether or not hypocalcemia could be caused by deficient vitamin D
activation to form the active 1,25 (OH)2 D hormone. This was rare with hypocalcemia
incidence rate due to low 1,25 (OH)2 D occurring in less than 10% of cows (Goff et al., 1989).
However, cows afflicted with milk fever in successive parturitions apparently do have delayed
1,25 (OH)2 D production and response. These cows also have greater plasma PTH in the days
surrounding parturition compared with cows that have not had a prior incidence of milk fever
(Goff et al., 1989). Interestingly, there may be a compounding negative influence of PTH on
vitamin D receptors (VDR; Reinhardt and Horst, 1990). Goff et al. (1995a) also observed a
slight decrease in VDR at time of calving when PTH activity would be elevated. How exactly
PTH and vitamin D metabolites influence each other and their receptors is not clearly
understood. Perhaps by providing enough vitamin D in the prepartum period to stimulate 1,25
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(OH)2 D production and VDR up-regulation, the negative effects of PTH at calving would not
be so detrimental to VDR numbers and 1,25 (OH)2 D stimulation.
Further action of vitamin D is thought to be indirectly involved in the occurrence of
hypocalcemia through VDR regulation around time of parturition (Goff et al., 1995a; Goff et al.,
1995b). For vitamin D to control Ca absorption efficiently it is important that VDRs are present
in adequate numbers and are effectively stimulated. It was thought that dairy cows with clinical
milk may have inadequate numbers of prepartum receptors for 1,25 (OH)2 D, the active
hormone needed for Ca uptake. Goff et al. (1995a) showed a significant increase in colon VDR
numbers in pregnant compared with non-pregnant Jersey cows, suggesting preparation for
lactational demands. However, there was no significant change in receptor numbers in the time
immediately around parturition. A slight decrease in receptor numbers at time of calving was
observed; although the reason for this decrease was unclear as complications with hypocalcemia
were an issue. Also observed was a delayed increase in VDR numbers of cows with a previous
history of milk fever; but, eventually typical numbers were reached. Liesegang et al. (2008)
explored the idea of decreased VDR function in third and greater lactation Holstein and Brown
Swiss cows compared with first and second lactation cows. There was no difference in
intestinal VDR numbers between breeds or as lactation number increased. Importantly, none of
the cows experienced periparturient hypocalcemia and all cows were in mid to late lactation at
time of sampling. The entire impact of VDRs around parturition is still unclear. There is an
obvious link between VDR existence and hypocalcemia (Beckman and DeLuca, 2002), though
how they are regulated during the cow’s transition period is not entirely clear. Other factors
affecting VDRs are thought to include DCAD (Goff et al., 1995a), VDR gene alterations
(Deiner et al., 2012), VDR anatomical locale (Beckman and DeLuca, 2002), and glucocorticoids
(Hidalgo et al., 2010). However, definitive evidence of the role of VDRs in hypocalcemia of
dairy cows has not been fully elucidated.
Controlling Hypocalcemia and Milk Fever
The ability to decrease incidence of hypocalcemia in dairy cows with greater susceptibility by
supplementing vitamin D during the close-up period is well documented. Julien et al. (1976)
demonstrated that cows of third and greater lactation with a prior history of milk fever were less
likely to develop milk fever during their subsequent lactation if injected with 10 million IU of
vitamin D3 1 wk prepartum. Furthermore, Hibbs and Conrad (1960) were able to increase
protection against milk fever in the more susceptible third and greater lactation Jersey cows by
as much as 38% by supplementing vitamin D (15 and 30 million IU/cow per d) as part of the
TMR or in capsule form for a week before calving. However, this protective effect of vitamin D
was not always observed (Taylor et al., 2008) and supplemental vitamin D benefits to cows
thought to be less susceptible is not well understood. These differences in response may be due
to a variety of reasons such as history of milk fever (Hibbs et al., 1976), parity, level of milk
production, or length of period of Ca stress (Muir et al., 1968). A low or negative DCAD during
the close-up period may very well play an important part in the effectiveness of vitamin D as
well (Wilkens et al., 2012).
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Supplementation
Whereas it is relatively unlikely for vitamin D to be deficient in most modern dairy farms, there
is reason to believe that supplemental vitamin D3 may be beneficial. Vitamin D2 and D3 can be
supplied orally or by intramuscular injection. Injection was thought to be more effective as the
vitamin would not be degraded in the rumen if given orally (Sommerfeldt et al., 1979).
However, Hymøller and Jensen (2010) reported no ruminal degradation of orally supplemented
vitamin D2 or D3. Drawbacks to using injectable vitamin D are optimal timing relative to actual
parturition, labor, and increased possibility of toxicosis. Because vitamin D is a fat-soluble
vitamin, it can accumulate in body tissues with frequent or large dose injections and result in
vitamin D toxicosis (Littledike and Horst, 1980). Tolerance of supplementary vitamin D by
injection can be 100 times less than to oral delivery (Littledike and Horst, 1980).
Vitamin D can be supplemented in its various plant and animal-derived forms (Sommerfeldt et
al., 1983; Taylor et al., 2008; Wilkens et al., 2012). It was suggested that vitamin D3
supplementation is more effective than vitamin D2 because vitamin D3 more efficiently
increased vitamin D blood metabolites (Sommerfeldt et al., 1983; Hymøller and Jensen, 2010).
Vitamin D3 is thought to be more effective at increasing vitamin D blood metabolites due to
differences in absorption mechanisms for D2 and D3 in the intestine (Sommerfeldt et al., 1983;
Hymøller and Jensen, 2010). Furthermore, Hymøller and Jensen (2011) suggested vitamin D2
supplementation might have a direct negative influence on D3 utilization in the body. Thus,
supplementing with vitamin D2 could be misleading when looking at the overall effects of
vitamin D supplementation on vitamin D plasma metabolite concentrations. Because vitamin
D3 is the naturally occurring form in animals and has the most biological activity, vitamin D3
supplementation is considered best.
The most efficacious amount of vitamin D3 needed by close-up and lactating dairy cows is not
clear. In general, 30 IU/kg of BW per d is recommended for cows in late pregnancy and early
lactation. For a 1600 lb cow, this is roughly equal to 20,000 IU/cow per d (NRC, 2001). Due to
the greater Ca demand of high producing cows, 30,000 to 40,000 IU/cow per d may improve Ca
absorption and milk production (NRC, 2001).
Appropriate timing of administration of vitamin D supplementation relative to actual calving
date can be difficult. Additionally, length of time of supplementation prior to calving to help
prevent hypocalcemia is unclear. Research referenced previously found positive results by D3
injection for about 1 wk before calving (Julien et al., 1976; Hibbs and Conrad, 1960). Taylor et
al. (2008) were able to increase blood 25 hydroxyvitamin D (25-OHD) after calving by orally
supplementing 600,000 IU of 25-OHD/cow per d in gel capsules within 6 d of calving, but there
was no increase in blood Ca around parturition. It is likely that for vitamin D supplementation
to work optimally all dietary and physiological conditions (i.e., acid-base status, dietary Ca,
VDRs) must be in alignment. Perhaps dietary supplementation of vitamin D at recommended
doses for a longer period of time (e.g., 20,000 IU/d for entire close-up period) would effectively
stimulate and up-regulate VDRs thus allowing for more efficient Ca absorption. This could
allow adequate time for vitamin D activation and subsequent stimulation of important biological
processes.
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RELATIONSHIPS WITH HEALTH AND REPRODUCTION
Periparturient Metabolic Disorders
Calcium is a major cellular signal needed for a range of biological functions (Jones, 2008). A
classic path analysis by Curtis et al. (1983) showed significant associations between poor Ca
status and muscle contraction-associated problems (i.e., dystocia and displaced abomasum) and
ketosis. Cows experiencing hypocalcemia spend 10% more time standing but less time at feed
and water in the days just before calving (Jawor et al., 2012). With decreased intake and
insufficient Ca for proper gut motility, risk of displaced abomasum postpartum increased (Curtis
et al., 1983). Furthermore, hypocalcemia predisposes cows to increased concentrations of
metabolites associated with ketosis. Both primiparous and multiparous cows fed a close-up diet
with a negative DCAD had decreased prepartum and postpartum blood non-esterified fatty acid
(NEFA) concentrations (DeGroot et al., 2010). The deleterious side effects of greater blood
NEFA concentrations and increased liver triglyceride accumulation might be reduced as a result
of the negative DCAD prepartum and suggests a possible reason to provide a negative DCAD
diet to close-up heifers (DeGroot et al., 2010). Others did not observe changes in peripartum
NEFA concentrations of cows provided an anion DCAD; perhaps changes in NEFA at this time
are more likely due to reduced DMI rather than the anionic diet per se (Ramos-Nieves et al.,
2009). Cows that develop hypocalcemia have greater NEFA concentrations than those that
maintain normal blood Ca; and, as a result those hypocalcemic cows are at greater risk of
developing ketosis (Reinhardt et al., 2011). Lower postpartum ketone β-hydroxybutyrate
(BHBA) concentrations were observed for cows that maintained normocalcemia (DeGroot et al.,
2010; Martinez et al., 2012).
Reproduction
In the USDA (2007) survey, approximately 79% of cows in the U. S. were culled for poor
reproductive performance. Through better control of periparturient Ca status, subsequent
reproductive management and success might be improved. Evidence to support this possibility
was first reported by Ward et al. (1970) who observed a decrease in number of days to first
ovulation postpartum by feeding 200 g Ca/d prepartum compared with 100 g/d. Additionally,
vitamin D supplementation decreased both days to first estrus and days to conception (Ward et
al., 1970). Calcium status is not thought to alter estrous cyclicity directly (Ward et al., 1970;
Martinez et al., 2012); however, cows that experience difficulty at parturition (i.e., dystocia,
stillbirth, and retained placenta) have reduced normal cyclicity (Martinez et al., 2012).
Furthermore, cows that maintain normal Ca status around parturition are more likely to have
increased pregnancy rate and reduced days open (Martinez et al., 2012). Also, Chapinal et al.
(2012) reported a link between incidence of periparturient disease and pregnancy rate. Cows
identified as being at greater risk for clinical diseases (i.e., increased blood NEFA and BHBA,
and(or) hypocalcemia) postpartum and dystocia had lower odds of pregnancy at first artificial
insemination (AI). Cows that maintained normal Ca status around parturition were 1.5 times
more likely to conceive at first AI.
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Immunity
Relationships between blood Ca concentrations and the cow’s ability to combat infections have
been established (Kimura et al., 2006; Nelson et al., 2010; Martinez et al., 2012). Calcium is an
important second messenger in the immune response. In an attempt to adjust the depleted Ca
pool during times of hypocalcemia, peripheral mononuclear cells release Ca from their stores.
In a short time these Ca stores are depleted and this limits the immune cells’ ability to send Ca
as a signal when triggered as an immune response (Kimura et al., 2006). Martinez et al. (2012)
linked greater risk of metritis with drops in serum Ca concentrations. Four times as many cows
developed metritis if they displayed both birthing problems (e.g., dystocia, twinning, stillbirths,
or retained placenta) and subclinical hypocalcemia compared with cows that did not have
birthing difficulties and maintained normal Ca status.
Inadequate vitamin D in the transition period compounds problems associated with
hypocalcemia by limiting the cow’s ability to increase Ca absorption and resorption (Goff and
Horst, 2003); thus, prolonging hypocalcemia and subsequent health problems. It has been
understood for a while that active vitamin D has a large role in immune function as a signal
hormone for monocytes (Reinhardt and Hustmyer, 1987). More recently, vitamin D has been
shown to be a crucial component of cow monocyte function (Nelson et al., 2010). Previously
this relationship between cow monocytes and vitamin D was not known. It is now understood
that monocytes not only have the ability to respond to active vitamin D, but also actually
produce the hormone (Nelson et al., 2010). The amount of vitamin D needed for appropriate
immune responses is unknown; it is simply assumed that the NRC (2001) recommended daily
intake is sufficient for all known biological needs. Given these recent findings, further
investigation into supplementation of vitamin D and increased dietary Ca in rations of sick
and(or) cows predisposed to hypocalcemia could prove beneficial.
CONCLUSIONS
Subclinical hypocalcemia and milk fever doubtless are detrimental disorders that affect mineral
element status, periparturient health, and lactational and reproductive performance of too many
dairy cows. Calcium status around parturition can be affected by a variety of factors surveyed
in this paper. Utilizing a low or negative DCAD in the close-up ration is a tried and often
effective way to increase blood Ca in the periparturient period. However, more proactive
approaches (i.e., reconsideration of “normal” blood Ca range, vitamin D supplementation, more
enhancement of immune function by modulating Ca status, diets tailored specifically to late
pregnant heifers, targeted approaches for predisposed cows) may prove efficacious and should
be considered. Together these findings highlight both the direct and indirect importance of Ca
status around parturition and how subsequent milk production and future performance and
profitability can be affected.
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Mastitis and Dairy Replacement Heifers: Management Practices
to Reduce the Odds
S.C. Nickerson
1, V.J. Eubanks
1,
J.D. Chapman
2, L.O. Ely,
1, K.P. Zanzalari
2, F.M. Kautz
1, D.J.
Hurley1, N.E. Forsberg
3, and Y.Q. Wang
3
1University of Georgia, Athens, GA,
2 Prince Agri Products Inc., Quincy, IL,
3OmniGen Research LLC, Corvallis, OR.
Corresponding author: [email protected]
SUMMARY
Prevalence of mastitis in unbred, breeding age, and pregnant dairy heifers is higher than
formerly realized. Infected mammary quarters, especially those with Staph. aureus IMI, exhibit
reduced mammary gland secretory potential, marked leukocyte infiltration, and the
accompanying inflammation. Both nonlactating and lactating commercial antibiotic infusion
products have been used successfully to cure existing infections and reduce SCC, and
nonlactating therapy prevents new IMI with environmental streptococci. However, the goal is
to prevent new infections from occurring in these young dairy animals through management
strategies aimed at vaccination, use of teat seals, fly control, and dietary supplementation.
Results of commercial vaccine trials illustrate that immunization will reduce Staph. aureus
mastitis in heifers at calving between approximately 45 and 60%, with reductions in SCC of
50%. Likewise, a fly control program for heifers will decrease incidence of Staph. aureus
mastitis by up to 83%. Lastly, dietary supplementation to boost the immune systems of heifers
has been shown to reduce incidence of mastitis at calving, lower SCC, and increase milk yield.
As global milk quality standards become more stringent, management practices based on curing
existing infections and preventing new IMI in heifers will ensure that these young dairy animals
enter the milking herd free of mastitis and with low SCC. Such practices should be considered
for incorporation into dairy herd health programs in herds suffering from a high prevalence of
heifer mastitis, especially that caused by Staph. aureus. Not only do these practices reduce new
infections in first calf heifers at parturition, they also reduce the introduction of Staph. aureus to
the milking herd.
INTRODUCTION
Replacement heifers are critical to dairy herd productivity because they represent the future
milking and breeding stock of all dairy operations. The goal should be to provide an
environment for heifers to develop their full lactation potential at the desired age with minimal
expense. Animal health and well-being play vital roles in achieving this potential, and one
disease that can influence future productivity is heifer mastitis caused by Staphylococcus
aureus, the coagulase-negative staphylococci (CNS), and the environmental streptococci. The
presence of mastitis in young dairy heifers is generally not observed until freshening or until the
first clinical flare-up in early lactation. Thus, animals may carry intramammary infections (IMI)
for a year or more before they are diagnosed with mastitis, resulting in reduced milk yield
(Boddie et al., 1987). The greatest development of milk-producing tissue in the udder occurs
during the first pregnancy, so it is important to protect the heifer mammary gland from
pathogenic microorganisms to ensure maximum milk production during the first and future
lactations.
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PREVALANCE IF MASTITIS IN UNBRED AND PREGNANT HEIFERS
The initial focus on heifer mastitis began in the mid 1980s after several dairy producers in
Louisiana complained to university researchers that a large percentage of their heifers were
freshening with clinical mastitis. Subsequent study of breeding age animals in a research herd
revealed that IMI were diagnosed as early as 6 months of age, and that infections persisted
throughout pregnancy and into lactation (Boddie et al., 1987). A follow-up study of 4
commercial herds demonstrated that IMI were found in 96.9% of heifers and in 74.6% of
mammary quarters (Trinidad et al., 1990a). Although the vast majority of udders were visually
healthy, 30% of udders and 15.1% of quarters showed clinical symptoms of mastitis as
evidenced by clots, flakes, and blood; only rarely were quarters swollen and enlarged. Staph.
aureus was isolated from 14.7% of quarters. This microorganism was also isolated from 25% of
quarters with clinical symptoms. Staph. aureus causes severe damage to mammary tissue, and
infections are very difficult to eliminate in lactating cows. Other organisms isolated from
secretions and percentage frequencies were Staph. chromogenes (43.1%). Staph. hyicus
(24.3%), other staphylococcal spp. (3.6%), Strep. dysgalactiae (0.4%), Strep. spp. (3.3%),
Nocardia species (0.4%), and mixed isolates containing staphylococci and streptococci (5.1%).
Figure 1. Although the majority of breeding age dairy heifers are healthy (a), up to 30% show
clinical symptoms of mastitis such as ropey, clotted secretions (b); however, enlarged, swollen
quarters are rare (c), thus, this disease is difficult to diagnose via visual observation of the
mammary gland.
MAMMARY LEUKOCYTE RESPONSE TO INTRAMAMMARY INFECTION
In lactating cows, the milk somatic cell count (SCC) is used as a measure of milk quality. This
count is composed mainly of leukocytes (macrophages, lymphocytes, and neutrophils, Figure 1)
and is considered an important parameter for assessing mammary health status (e.g.
inflammation). It is well known that milk yield decreases as the SCC and the incidence of
mastitis increases. Thus, SCC in breeding age and pregnant heifer mammary gland secretions
have been analyzed to measure the degree of inflammation and potential reductions in future
milk yield. In a study by Boddie et al. (1987), the mean SCC of quarters from unbred heifers
infected with Staph. chromogenes, Staph. hyicus, and Staph. aureus were 7.8, 8.5, and 9.2 x
106/ml, respectively, whereas the mean SCC of uninfected quarters was 3.5 x 10
6.
Approximately 13% of quarter secretions sampled prepartum contained Staph. aureus, and after
a b c
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freshening, the SCC of these quarters averaged 578 x 103/ml, a cell count associated with a loss
of greater than 4.4 lb of milk/day.
Figure 2. The somatic cell count includes macrophages (M), lymphocytes (L), and neutrophils
(N).
The volume of mammary secretion is very low in breeding-age animals; thus, somatic cells
become concentrated, resulting in high SCCs even in uninfected quarters. Such elevated SCC
over a long period of time suggests that mammary tissues in affected quarters are in a state of
chronic inflammation, which could adversely affect development of milk-producing tissues and
negatively affect future milk yield. In response to infection, neutrophils become the major
leukocyte type that infiltrates mammary tissue from the vascular system to phagocytose and kill
mastitis-causing bacteria. The migration of neutrophils across the mammary epithelium causes
mechanical as well as chemical damage to the milk secretory cells resulting in decreased yield
(Akers and Nickerson, 2011).
MAMMARY TISSUE RESPONSE TO PRESENCE OF INFECTION
Histologic observations of mammary tissue samples from uninfected quarters of heifers by
Trinidad et al. (1990a) showed that milk-producing alveoli were small; the epithelial lining was
composed of a single layer of cuboidal cells surrounding a small luminal space with little or no
stained secretory product (Figure 3a). Interalveolar connective tissue area comprised
approximately half of the observed tissue area. Mammary tissues infected with Staph. aureus,
on the other hand, exhibited large amounts of interalveolar connective tissues and reductions in
epithelial and luminal areas (Figure 3b), suggesting reduced secretory activity. Indeed, results of
morphometric analysis showed that percentages of alveolar epithelium and lumen in quarters
infected with Staph. aureus were lower (P < .05) than those in uninfected quarters. Quarters
infected with Staph. aureus also showed a greater percentage (P < .05) of interalveolar stroma
than did uninfected quarters. Additionally, quarters infected with Staph. aureus exhibited
M
N
L
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significantly greater infiltration of leukocytes (mainly lymphocytes and neutrophils) compared
with uninfected tissues.
The greatest development of secretory tissues in young heifers occurs during the first pregnancy,
and these tissues are affected adversely by bacterial infection and inflammation, leading to
deposition of connective tissue instead of milk secretory tissue, which results in a reduction of
future milk yield.
Figure 3a. Portion of mammary parenchymal tissue typical of that obtained from uninfected
quarters exhibiting small milk-producing alveoli (A) with empty, ovoid lumens (1), lumens with
some secretions (2), and interalveolar connective tissue stroma (S). x180.
Figure 3b. Parenchymal tissue from a quarter infected with Staph. aureus exhibiting a large
percentage of interalveolar connective tissue stroma (S), fewer numbers of alveoli (A), and
limited alveolar luminal areas (L). D = Duct. x180.
USE OF ANTIBIOTIC THERAPY TO CONTROL MAMMARY INFECTIONS
Curing Existing Cases of Mastitis with Nonlactating Cow Antibiotic Therapy
Because of the high level of infection found in breeding age and pregnant heifers, especially
mastitis caused by Staph. aureus, antimicrobial therapy should be considered. In an initial study
to evaluate the effectiveness of treatment, several heifers from 4 commercial herds were
randomly selected to receive a single intramammary treatment of a penicillin and
dihydrostreptomycin product into all 4 mammary quarters (Trinidad et al., 1990b). Treatments
a b
A
S A
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were made at approximately 60 days prior to calving. Results showed that 97.1% of treated
heifers (n = 35) were infected with some type of mastitis at the time of treatment, but, at calving,
only 40% remained infected. Of the untreated control heifers (n = 38), 100% were infected at
initial sampling, and at calving, mastitis was reduced only slightly to 97.4%. Staph. aureus was
isolated from 11 quarters of 6 treated heifers before antibiotic infusion (45.8%), but at calving,
this organism was isolated from only 1 quarter of 1 heifer (4.2%). In the control group, 18
quarters of 10 heifers were infected with Staph. aureus at time of treatment (45%). At calving,
6 of the control heifers still had Staph. aureus mastitis in 11 quarters (55%). Thus, the overall
incidence of IMI caused by Staph. aureus was reduced over 90% and SCC were reduced by
50%. Production data collected over the first 2 months of lactation demonstrated that Staph.
aureus-infected heifers receiving nonlactating cow therapy during pregnancy produced an
average of 5.5 lb more milk per day (or 10% more milk) than Staph. aureus-infected herd mates
that did not receive treatment. Other advantages include a longer productive life and higher
income due to lower SCC and higher quality milk premiums.
Subsequent studies (Owens et al., 1991, 1994) confirmed results of the initial investigation
above. Heifers that were infected with Staph. aureus were infused 8-12 weeks prepartum with
one dose of 300 mg of a cephapirin benzathine product into all 4 mammary quarters and were
compared with untreated controls infected with Staph. aureus. Results demonstrated cure rates
between 87 and 100%. After antibiotic infusion, SCC in infected quarters that cured decreased
from 15 x 106/ml to 4 x 10
6/ml 1 week later, and to 700 x 10
3/ml at calving, whereas SCC in
untreated controls at calving were 5 x 106/ml. Treated heifers in which Staph. aureus IMI were
cured yielded 11% more milk during the first 2 months of lactation. One of these studies also
demonstrated that prepartum treatment served as a prophylactic against new cases of
environmental strep mastitis (Owens et al., 1994), reducing the new IMI rate at calving by 93%.
Thus, use of nonlactating cow therapy was effective in preventing new IMI as well as curing
existing infections.
When Is the Best Time to Administer Nonlactating Cow Therapy?
To answer this question, a 2-year study was conducted (Owens et al., 2001) in which 233 Jersey
heifers were quarter sampled shortly after they were confirmed pregnant and at 4-week intervals
thereafter. At the initial sampling, 56.5% of quarters were infected with some type of organism,
and 15.4% of quarters were infected with Staph. aureus. After the initial sampling, animals were
treated with a one-time infusion of 1 of 5 different nonlactating cow infusion products during
the first (0 - 90 days), second (91 - 180 days), or third (181 - 270 days) trimester of pregnancy.
Results showed that cure rates for the 5 products were high, ranging from 67 to 100%, and
significantly higher than the spontaneous cure rate (25%) observed in untreated control quarters;
no differences were observed among the three treatment time periods during gestation. Thus, the
timing of treatment is best determined by what is most convenient for the management practices
of a particular dairy. For example, heifers could be treated: 1) at time of artificial insemination;
2) during routine rectal palpation to determine pregnancy status; or 3) when moved to a new
location in preparation for calving. Treatment should be administered no less than 45 days prior
to expected calving date to prevent antibiotic residues.
When administering treatment, it is important to 1) restrain the heifer in a headlock and/or
squeeze chute, and if necessary further restrain the animal by “tailing”; 2) sanitize the teat
orifice with cotton balls or pads soaked in 70% alcohol; 3) use the partial insertion technique
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when inserting the tip of the syringe cannula (only 2-3 mm) into the teat canal; and 4) dip teats
in a germicide to kill any contaminating bacteria. See Figure 4.
The treatment of heifers during pregnancy with a nonlactating cow product is advantageous
because: 1) the cure rate is higher than during lactation, especially against Staph. aureus; 2)
there are no milk losses during therapy; 3) the risk of antibiotic residues is minimal; 4) SCC at
calving is reduced; 5) new IMI with environmental streptococci is prevented; and 6) milk
production is increased by approximately 10% in successfully treated animals.
Figure 4. a) Securing the animal in a headlock system while feeding helps to immobilize the
heifer. b) Teats should be sanitized prior to treatment. c) When infusing antibiotic, only the tip
of the syringe cannula should be inserted into the teat orifice. d) After therapy, teats should be
immersed in an effective germicide.
Efficacy of Lactating Cow Products in Curing IMI
Lactating cow products also have been used successfully in heifers when treating infections
caused by the environmental streptococci and CNS immediately prior to calving. Studies on
this subject have been performed in late gestation 1 - 3 weeks before calving. Although treating
animals 1 week prior to calving is successful, antibiotic residues often result, so most trials have
focused on treating 2-3 weeks prepartum.
For example, Oliver et al. (2004) conducted a trial to determine if therapy with penicillin-
novobiocin or pirlimycin hydrochloride 2 weeks prepartum was effective in curing IMI and
thereby reducing the level of mastitis during early lactation. Approximately 73% of Holstein
heifers were infected 14 days before expected calving; the majority of IMI were due to CNS
(44%) and Staph. aureus (30%). At calving, the cure rate was 76% after treatment with
penicillin-novobiocin, and 59% following treatment with pirlimycin. In this same study, 96% of
Jersey heifers were infected 14 days before calving; the majority of IMI were due to CNS
(61%), Strep. spp. (19%), and Staph. aureus (8%). At calving, the cure rate was 75% after
treatment with penicillin-novobiocin, and 87% following treatment with pirlimycin. Thus,
prepartum therapy of heifer mammary glands with penicillin-novobiocin or pirlimycin
hydrochloride was effective in reducing the percentage of heifers infected with mastitis
pathogens during early lactation.
a b c d
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As a part of the above trial, milk production and somatic cell count data from 82 control heifers
and 111 heifers treated with antibiotics before calving were evaluated (Oliver et al., 2003). Milk
production was about 10% higher in heifers treated prepartum with antibiotics. Additionally,
treated heifers had significantly lower SCCs than control heifers (~52,000 vs. 81,000). Thus,
prepartum antibiotic treatment to reduce the rate of mastitis in heifers during early lactation was
economically beneficial.
The studies on prepartum treatment with lactating cow therapy administered 7 - 21 days before
calving have shown treatment to be effective for quarters infected with CNS and Strep. uberis,
but waiting until this time to treat chronic Staph. aureus mastitis might be too late. A mammary
gland that has been infected with Staph. aureus for several months to a year will not develop
normally, and treatment during the immediate prepartum period would most likely be of little
benefit in curing infections or salvaging mammary tissue. At this point, the tissue damage
would have already been done, and affected quarters should have been treated earlier in
gestation to: 1) cure existing infections; 2) reduce chronic inflammation; and 3) allow mammary
tissue to develop normally during the later stages of pregnancy.
Results of these trials demonstrated that nonlactating and lactating cow antimicrobial treatment
of heifers, known to be at risk for developing IMI, is advantageous because the cure rate is
much higher than that obtained when treating infections during lactation. In addition, most
studies show that SCC are lower, there is no milk loss due to therapy, risk of antibiotic residue
at calving is minimal, and future milk production is increased in heifers cured of IMI. However,
the goal in controlling mastitis is to prevent new infections, and management strategies to
enhance disease prevention are discussed below.
MANAGING HEIFERS TO PREVENT MAMMARY INFECTIONS
Role of Vaccination in Mastitis Control
Although antimicrobial therapy is successful in curing existing cases of mastitis, the goal from a
herd management perspective is to prevent new infections from occurring, and vaccination has
been attempted as a prophylactic measure. The purpose of vaccination is to increase circulating
antibodies directed against certain mastitis pathogens to protect against bacterial invasion.
Researchers in Louisiana evaluated a commercially available Staph. aureus vaccine in young
dairy animals (Nickerson et al., 1999). This product is the only Staph. aureus vaccine on the
market in the US (Lysigin®, Boehringer Ingelheim Vetmedica, Inc., St. Joseph, MO, USA). At
6 months of age, 35 Jersey heifers were vaccinated following manufacturer’s instructions using
a 5-ml dose intramuscularly in the semimembranosus muscle (upper thigh) of the rear leg
(Figure 5), and 14 days later, animals received a booster dose, which was repeated at 6-month
intervals. Another 35 heifers served as unvaccinated controls. Note: Injections were
administered per label instructions; however, it is generally recommended to avoid muscle
tissues in the leg, thereby minimizing potential abscess formation; injection into the neck region
is preferable. Results demonstrated that: 1) the number of quarters exhibiting chronic Staph.
aureus mastitis during pregnancy was reduced 43.1% in vaccinates compared with controls; 2)
rate of new IMI during pregnancy was reduced 44.8%; 3) rate of new IMI at freshening was
reduced 44.7%; and 4) the SCC was reduced by 50% in vaccinates compared with controls.
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Figure 5. Vaccination (5 cc) into the left semimembranosus muscle of the rear leg using an
18-gauge needle.
In a subsequent, more in depth study using the same vaccine (Lysigin®), 106 Holstein heifers
from a dairy herd in Virginia were evaluated (Nickerson et al., 2009). Previous microbiological
culture of heifer mammary secretions indicated that approximately 35% of the animals were
infected with Staph. aureus. At 6 to 18 months of age, 53 heifers were vaccinated and boosted
as above, and the other 53 heifers served as unvaccinated controls. The purpose was to
determine if vaccination reduced the level of Staph. aureus at calving as observed in the
Louisiana trial.
Vaccine efficacy data showed that the percentage of heifers with Staph. aureus IMI at
freshening was lower in vaccinates (13.3%) compared with controls (34.0%); a reduction of
60.9%. Likewise, an examination of health records showed that the percentage of heifers that
were culled or died during the trial was reduced by approximately one-third by vaccination:
16.9% in vaccinates and 24.5% in controls. Somatic cell counts in samples collected during first
week of lactation from uninfected heifers for vaccinates and controls were 66,095 and
132,754/ml, respectively; a 50.2% reduction; and for infected heifers, SCC were 441,764 and
892,176/ml, respectively; a 50.5% reduction.
An examination of the 305-day lactation milk yield for the 1st lactation of both vaccinated and
unvaccinated control heifers demonstrated an approximate 10% increase in production in
vaccinates vs. controls (24,250 vs. 22,046 lb, respectively) or a difference of 2,204 lb. Likewise,
the 305-day pounds of both fat and protein were higher in vaccinates than controls (fat: 899 vs.
747 kg, respectively; protein: 727 vs. 694 kg, respectively). An examination of the number of
days in milk for the first lactation demonstrated that vaccinates lactated 13 days longer than the
unvaccinated controls (349 vs. 336 days). In addition, average first lactation SCC were 11,000
cells/ml lower in vaccinates compared with controls (49,000 vs. 60,000/ml).
Results of this Virginia investigation demonstrated that vaccinating dairy heifers according to
the prescribed protocol with a commercial USDA licensed Staph. aureus bacterin, Lysigin®
,
reduced the number of new Staph. aureus intramammary infections at time of calving by 60.9%,
lowered the SCC by 50%, and decreased the culling rate by approximately one-third. In
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addition, overall milk yield, production of fat and protein, and number of days in milk were
greater in vaccinated heifers compared with controls. This prevention strategy may represent a
major control mechanism for managing Staph. aureus in the future, especially as new antigens
and adjuvants are added to vaccine preparations.
Efficacy of an Infusible Teat Seal for Preventing IMI
Because bacteria breach the teat canal to cause infection, products have been developed to serve
as barrier to bacterial entry or seal the teat canal against infection. Such products form a
physical plug in the distal teat cistern and teat canal (Figure 6). In one study involving 255
pregnant heifers, mammary quarters were treated approximately 1 month prepartum with an
infusible teat seal composed of bismuth subnitrate. Results showed that this procedure 1)
reduced the risk of new IMI with any organism by 74%, 2) reduced the prevalence of post
calving IMI by 65%; 3) reduced the risk of Strep. uberis infection in quarters with an IMI pre-
calving by 70%; and 4) reduced the incidence of clinical mastitis from which a pathogen was
isolated by 70% in quarters detected with an IMI pre-calving (Parker et al., 2007). In a
subsequent trial, 1,067 bred heifers were treated approximately 1 month prepartum with teat
seal, and results demonstrated that treatment 1) reduced the risk of clinical mastitis by 68%, and
2) reduced the risk of IMI due to Strep. uberis by 84% (Parker et al., 2008).
Although teat seal contains no antibiotic and cannot cure existing infections, this product is
effective in preventing new cases of mastitis, especially those caused by Strep. uberis. It is
emphasized that to be effective, teat seal should be administered approximately 30 days prior to
calving and that strict teat end hygiene be followed when applying teat seal products.
Figure 6. Radiograph of a teat infused with teat seal, illustrating the teat seal material in the
distal teat cistern and in the teat canal (arrows).
The Role of Horn Flies in the Development of Heifer Mastitis
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Historically, the major association between flies and intramammary infections has been with the
development of summer mastitis, in which the biting fly, Hydrotoea irritans, is the proven
vector. Summer mastitis is an isolated seasonal problem primarily in July, August, and
September in heifers and dry cows of northern Europe, and may be controlled by insecticidal
sprays. In the US, fly control is used to reduce these insect pests on farm premises, and
subsequently reduce animal stress, but its application as an adjunct management practice for
preventing new cases of mastitis and reducing SCC has not been considered or embraced by
producers.
An initial survey performed at Louisiana State University showed that prevalence of mastitis in
bred heifers was significantly lower in dairy herds that used some form of fly control for their
lactating cows, dry cows, and heifers compared with herds applying no fly control (Figure 7)
(Nickerson et al., 1995). The greatest reductions were in numbers of Staph. aureus and the
environmental streptococci, both major mastitis pathogens in adult cows associated with
elevations in SCC.
The particular species of fly associated with mastitis is the blood-sucking horn fly (Haematobia
irritans). This species is commonly found on the backs of dairy animals (Figure 8a), preferring
a dark hair coat, but will also attack the teats, leading to the development of mastitis, especially
among dairy heifers. Results of the survey above (Nickerson et al., 1995) also demonstrated
that bred heifers having teats with bite lesions and scabs caused by horn flies exhibited a 70%
frequency of intramammary infection compared with a 40% frequency in heifers with normal
teats free of lesions. Such infections are always associated with elevated SCC in excess of 5
million/ml in these young animals. Horn flies tend to attack front teats rather than rear teats. See
Figure 8b below illustrating horn flies and lesions on heifer teats.
Figure 7. Prevalence of mastitis in Louisiana dairy herds with and without a fly control
program.
32.9
5.6 3.7
44.4 41.4
55.2
20.7
100
0102030405060708090
100
CNS S. aureus Env. Streps Total
Per
cen
t
Mastitis-causing pathogen
With fly control W/o fly control
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Figure 8. a) Horn flies on the back of a Holstein heifer; note preference for dark hair color vs.
white hair. b) Udder of a 10-month-old heifer illustrating horn flies (arrows) and lesions on teat
ends.
Since that first survey, researchers have proven through DNA studies that the horn fly is not
only responsible for teat lesions on heifers, but is indeed a vector in the transmission of mastitis-
causing bacteria such as Staph. aureus, from heifer to heifer, especially during the warm and
humid months of the year (Owens at al., 1998). Such mastitic heifers serve as sources of IMI
for transmission to the entire lactating and nonlactating herds.
How Can Flies Be Controlled to Manage Heifer Mastitis?
Once it was established that the horn fly was a vector in the transmission of mastitis-causing
bacteria, the next step was to develop management practices to reduce flies and lower the
prevalence of intramammary infections. Insecticide-impregnated tags placed on the tail switch
in close proximity to the udder during the spring and summer months were successful in
reducing horn fly populations by 60% as well as the incidence of mastitis during the first 2
months after placement. However, after 2 months, tags fell off and replacing them was
impractical from a management standpoint (Nickerson et al, 1997). In a subsequent trial, the
daily dietary supplementation of an insect growth regulator helped to suppress fly populations
but not enough to prevent new cases of mastitis in dairy heifers (Owens et al., 2000). However,
the use of an insecticidal pour-on every 2 weeks for 6 weeks followed by treatment with
insecticidal ear tags reduced fly populations and decreased the incidence of new Staph. aureus
by 83% during a 6-mo trial in heifers during the warm season in Louisiana (Owens et al., 2002).
More recently, an ongoing trial at UGA has found that the use of a pour-on every 2 to 4 weeks
drastically reduced fly populations, allowing teats to heal, and reducing two important sources
of S. aureus: flies and teat lesions.
b a
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These studies demonstrate that, during the warm and humid months of the year, horn flies do
serve as vectors in the transmission of heifer mastitis, which is associated with elevated SCC in
these young dairy animals. Although research has not been conducted to show this same
association in lactating and dry adult cows, it is assumed that fly populations play some role in
the elevation of mastitis and SCC observed in the hot summer months. And, with the proposed
reduction in the SCC legal limit to 400,000/ml in the USA, and in light of the fact that milk
buyers are imposing their own limits, some as low as 250,000/ml, it is imperative that dairymen
utilize all possible means to prevent new cases of mastitis and their associated SCC. A simple
fly control program can serve as an important adjunct to an overall herd plan of mastitis control
and assist dairymen in lowering their bulk tank SCC and earning quality premiums for their
products.
Influence of Dietary Supplementation on Mammary Health
Another management tool to reduce the level of infection and SCC when heifers calve, as well
as throughout lactation, is through dietary supplementation. Diet plays a role in udder resistance
to infection because certain nutrients affect various mammary resistance mechanisms, namely:
(1) leukocyte function, (2) antibody transport, and (3) mammary tissue integrity. In one study,
heifers received selenium (0.3 ppm/day) and vitamin E (50 to 100 ppm/day) supplementation
starting 60 days prepartum and throughout lactation, and a selenium booster injection (50 mg)
was administered 21 days prior to freshening (Hogan et al., 1993). This protocol reduced
staphylococcal and coliform infections at calving by 42%, and duration of infection was reduced
40 to 50% in supplemented heifers. Clinical mastitis in supplemented heifers was reduced 57%
in early lactation and 3.2% throughout lactation, and the mean SCC was lower. Thus, vitamin E
and selenium improved udder health of heifers, and the effect of dietary supplementation was
most evident at calving and in early lactation.
In a more recent study (Eubanks et al., 2012), dairy heifers (n = 40) were fed a daily supplement
beginning at 5 months of age containing an immune modulator (OmniGen-AF®), which included
a proprietary mixture of B-complex vitamins and yeast extract. Blood profile data collected
during gestation showed that compared with unsupplemented control animals (n = 40), those
supplemented with the immune modulator exhibited greater leukocyte expression of L-selectin
and interleukin-8 cell surface receptors, as well as greater leukocyte phagocytic activity and
production of reactive oxygen species, suggesting the capability for a greater immune response
to bacterial infection.
To date, additional data has been collected on 24 heifers that have calved. On a mammary
quarter basis, prevalence of mastitis among quarters at 30-60 d prepartum was similar between
treatment groups (58.3% vs. 52.5%); however, prevalence among quarters at 3 d postpartum
was 1.8-fold lower in OmniGen-AF®-supplemented animals (2.8%) compared to controls
(5.1%), and by 10 d postpartum, there was no change in mastitis prevalence among quarters in
supplemented animals (2.8%), but prevalence was 2.7-fold higher in quarters of unsupplemented
controls (7.5%) (Figure 9).
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Figure 9. Pre- and postpartum prevalence (%) of mastitis among mammary quarters of
OmniGen-AF®-supplemented and control heifers.
Similarly, SCC remained lower in supplemented vs. control heifers (Figure 10). At 3 d
postpartum, average SCC for OmniGen-AF®-supplemented heifers was 221,000/ml vs.
535,000/ml for controls. By 10d postpartum, SCC in supplemented heifers had fallen to
183,000/ml, but SCC remained elevated 2.4-fold in controls (441,000/ml).
Figure 10. Three- and 10-d postpartum SCC among mammary quarters of OmniGen-AF®-
supplemented and control heifers.
0
50
100
30-60dPrepartum
3dPostpartum
10dPostpartum
58.3
2.8 2.8
52.5
5.1 7.5
Supplemented Control
0200400600
3d Postpartum 10dPostpartum
221 183
535 441
Supplemented Control
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Interestingly, both supplemented and control heifers entered lactation producing a similar milk
yield, although supplemented animal yield (24 lb) was slightly greater than controls (23 lb) (Wk
0, Figure 11); however, during the first few weeks of lactation (the most susceptible time period
for development of new IMI), OmniGen-AF®-supplemented heifers appeared to remain healthier
(less mastitis, lower SCC), and progressively produced a greater daily milk yield than
unsupplemented controls through wk 5 postpartum. For example, by wk 1, supplemented heifers
were producing an average of 2.4 lb per day more milk than controls, by wk 3, this difference
was 7.7 lb, and at wk 5, the difference between OmniGen-AF®-supplemented and control
animals was still 7 lb.
Figure 11. Milk production over the first 5 wk of lactation in OmniGen-AF®-supplemented and
control heifers.
Overall, postpartum results showed that animals supplemented with OmniGen-AF® exhibited
increased milk production, decreased prevalence of mastitis, and decreased SCC compared with
control heifers, indicating a positive effect of feeding the feed supplement. While differences in
mastitis prevalence and SCC were not observed prepartum, the postpartum differences observed
between OmniGen-AF®-supplemented and control cows suggest a positive effect on the immune
system after feeding the dietary supplement as heifers, which was manifested during the
periparturient period (at time of stress), or more specifically, during the first few days
postpartum when animals are subjected to increased risk of IMI, elevated SCC, and decreased
production.
24
51.7 56.5
63.8 68.9 68.4
23
49.3 53.1
56.1 59.2 61.4
0
10
20
30
40
50
60
70
80
Week 0 Week 1 Week 2 Week 3 Week 4 Week 5
Supplemented Control
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REFERENCES
Akers, R.M. and S.C. Nickerson. 2011. Invited review. Mastitis and its impact on structure and
function in the ruminant mammary gland. Journal of Mammary Gland Biology and
Neoplasia. 16:275-289.
Boddie, R.L., S.C. Nickerson, W.E. Owens and J.L.Watts. 1987. Udder microflora in
nonlactating heifers. Agri-Practice, Vol.8, pp. 22-25.
Eubanks V.J., D.J. Hurley, L.O. Ely, F.M. Kautz, S.C. Nickerson, N.E. Forsberg, Y.Q. Wang,
K. Zanzalari and J. Chapman. 2012. Pre- and postpartum immunomodulatory effects of
a dietary supplement on the immune system of dairy heifers. J. Anim. Sci. Vol. 90,
Suppl. 3/J. Dairy Sci. Vol. 95, Suppl. 2. Abstr #220, pg. 222.
Hogan, J.S., W.P. Weiss and K.L. Smith. 1993. Role of vitamin E and selenium in the host
defense responses to mastitis. Journal of Dairy Science, Vol.76, pp. 2795-2802.
Nickerson, S.C., W.E. Owens and R.L. Boddie. 1995. Mastitis in dairy heifers: initial studies on
prevalence and control. Journal of Dairy Science, Vol.78, pp. 1607-1618.
Nickerson, S.C., W.E. Owens, S.M. DeRouen, R.L. Boddie and G.M. Tomita. 1997. Use of
insecticide impregnated tail tags may reduce incidence of mastitis in beef cows. The
Louisiana Cattleman. August, Pages 11-14.
Nickerson, S.C., W.E. Owens, G.M. Tomita and P.W. Widel. 1999. Vaccinating dairy heifers
with a Staphylococcus aureus bacterin reduces mastitis at calving. Large Animal
Practice, Vol.20, pp. 16-20.
Nickerson, S.C., L.O. Ely, E.P. Hovingh and P.W. Widel. 2009. Immunizing dairy heifers
can reduce prevalence of Staphylococcus aureus and reduce herd somatic cell counts.
In: Dairy Cattle Mastitis and Milking Management,
DAIReXNET.
<http://www.extension.org/pages/Dairy_Cattle_Mastitis_and_Milking_Managemnt>.
Oliver, S.P., M.J. Lewis, B.E. Gillespie, H.H. Dowlen, E.C. Janicke and R.K. Roberts. 2003.
Milk production, milk quality and economic benefit associated with prepartum
Antibiotic treatment of heifers. Journal of Dairy Science, Vol.86, pp. 1187-1193.
Oliver, S.P., S.J. Ivey, B.E. Gillespie, M.J. Lewis, D.L Johnson, K.C Lamar, H. Moorehead,
H.H. Dowlen, S.T. Chester and J.W. Hallberg. 2004. Influence of prepartum
intramammary infusion of pirlimycin hydrochloride or penicillin-novobiocin on
mastitis in heifers during early lactation. Journal of Dairy Science, Vol.87, pp. 1727-
1731.
Owens, W.E., S.C. Nickerson and R.L. Boddie. 2000. The effect of methoprene on horn fly
numbers and mastitis in dairy heifers. Large Animal Practice, Vol.21, pp. 26-28.
Owens, W.E., S.C. Nickerson, R.L. Boddie, G.M. Tomita and C.H. Ray. 2001. Prevalence of
mastitis in dairy heifers and effectiveness of antibiotic therapy. Journal of Dairy
Science, Vol.84, pp. 814-817.
Owens, W.E., S.C. Nickerson, P.J. Washburn and C.H. Ray. 1991. Efficacy of a cephapirin dry
cow product for treatment of experimentally induced Staphylococcus aureus mastitis
in heifers. Journal of Dairy Science, Vol.74, pp. 3376-3382.
Owens, W.E., S.C. Nickerson, P.J. Washburn and C.H. Ray. 1994. Prepartum antibiotic
therapy with a cephapirin dry cow product against naturally occurring intramammary
infections in heifers. Veterinary Medicine Series B, Vol.41, pp. 90-100.
Owens, W.E., S.P. Oliver, B.E. Gillespie, C.H. Ray and S.C. Nickerson. 1998. Role of horn
Flies (Haematobia irritans) in Staphylococcus aureus-induced mastitis in dairy
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34
heifers. American Journal of Veterinary Research, Vol.59, pp.1122-1124.
Owens, W.E., S.C. Nickerson and C.H. Ray. 2002. Effect of a pour-on and fly tag insecticide
combination in controlling horn flies and Staphylococcus aureus mastitis in dairy
heifers. 2002 Louisiana Dairy Report. Baton Rouge, Louisiana, USA, pp. 39-42.
Parker, K.I., C. Compton, F.M. Anniss, A. Weir, C. Heuer and S. McDougall. 2007. Subclinical
and clinical mastitis in heifers following the use of a teat sealant precalving. J. Dairy
Science, 90: 207-218.
Parker, K.I., C. Compton, F.M. Anniss, C. Heuer and S. McDougall. 2008. Quarter level
analysis of subclinical and clinical mastitis in primiparous heifers following the use
of a teat sealant or an injectable antibiotic, or both, precalving. J. Dairy Science, 91:
169-181.
Trinidad, P., S.C. Nickerson and R.W. Adkinson. 1990a. Histopathology of staphylococcal
mastitis in unbred dairy heifers. Journal of Dairy Science, Vol.73, pp. 639-647.
Trinidad, P., S.C. Nickerson, T.K. Alley and R.W. Adkinson. 1990b. Efficacy of
intramammary treatment in unbred and primigravid dairy heifers. Journal of the
American Veterinary Medical Association, Vol.197, pp. 465-470.
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The Physiology of Stress and Effects on Immune Health in Ruminants
J.A. Carroll*, and N.C. Burdick Sanchez
Livestock Issues Research Unit
USDA-ARS
Corresponding author: [email protected]
SUMMARY
As researchers have continued to explore the complex interactions among stress and
production parameters such as growth, feed efficiency, and health, multidisciplinary efforts
have emerged leading to a greater understanding of homeostatic regulation.
The immune system can be regulated by several different endocrine secretions, with the
most prominent being those secreted in response to stress.
Ultimately, within the animal, the immune system response to stress is dependent upon the
type of stress encountered (i.e., acute versus chronic).
Given that the innate immune system provides the first line of defense, understanding the
effects of stress hormones on innate immunity holds a great deal of potential with regard to
improving cattle health, and ultimately productivity.
INTRODUCTION
Livestock are exposed to stress at various points during production. Examples include weaning,
the transportation process, and castration and other less appreciated stressors such as extreme
fluctuations in temperature, poor nutrition, and mixing of unfamiliar animals. It has been well
established that stress can influence how an animal responds and recovers from exposure to
pathogens, and therefore, it is essential that animals have a well-developed and properly
functioning immune system. While chronic stress negatively impacts immunity, literature has
demonstrated that acute stress can potentially prime the immune system (Dhabhar, 2000;
Dhabhar, 2009). Animals that possess an adequate level of immunological protection have been
demonstrated to exhibit greater reproductive capabilities, enhanced growth, and increased feed
efficiency (Galyean et al., 1999).
* Mention of trade names or commercial products in this article is solely for the purpose of
providing specific information and does not imply recommendation or endorsement by the U.S.
Department of Agriculture. The U.S. Department of Agriculture (USDA) prohibits
discrimination in all its programs and activities on the basis of race, color, national origin, age,
disability, and where applicable, sex, marital status, familial status, parental status, religion,
sexual orientation, genetic information, political beliefs, reprisal, or because all or part of an
individual's income is derived from any public assistance program. (Not all prohibited bases
apply to all programs.) Persons with disabilities who require alternative means for
communication of program information (Braille, large print, audiotape, etc.) should contact
USDA's TARGET Center at (202) 720-2600 (voice and TDD). To file a complaint of
discrimination, write to USDA, Director, Office of Civil Rights, 1400 Independence Avenue,
S.W., Washington, D.C. 20250-9410, or call (800) 795-3272 (voice) or (202) 720-6382 (TDD).
USDA is an equal opportunity provider and employer.
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As researchers have continued to explore the complex interactions among stress and production
parameters such as growth, feed efficiency, and health, multidisciplinary efforts have emerged
leading to a greater understanding of homeostatic regulation. Additionally, there has been an
increased effort to elucidate the interactions between stress responsiveness and immunological
parameters in animals that may be either predisposed to or resistant to the detrimental effects of
stress due to factors such as genetic programming, management practices and (or) prior
experiences.
Today, the scientific community and producers alike acknowledge the fact that “stress” can
potentially have detrimental effects on animal productivity, and overall health and well-being.
Even though the debate among animal scientists concerning the definition and quantification of
“stress” is ongoing, an increased understanding and appreciation with regard to the effects of
“stress” on livestock production now exists both within the scientific community and with
livestock producers. While the physiological consequences of “stress” on the body have been of
scientific interest for many years, scientists have yet to fully elucidate the complex interactions
among stress hormones and the immune system. However, there is substantial literature
available documenting the detrimental effects of prolonged stress on the immune system and
overall health of livestock.
STRESS
Stress, as it relates to bodily functions, has been defined as the sum of all biological reactions to
physical, emotional, or mental stimuli that disturb an individual’s homeostasis (Pacák and
Palkovits, 2001). Therefore, a stressor can be defined as any internal or external stimuli or threat
that disrupts homeostasis of the body, and elicits a coordinated physiological response (stress
response) in an attempt to reestablish homeostasis. Maintaining a state of homeostasis requires
proper functioning of all physiological processes including the stress and immune systems
which are influenced by numerous factors including environmental conditions, pathogen
exposure, genetic makeup, animal temperament, and nutrient availability. Research related to
“stress” in domestic animals continues to evolve and expand, with emergent multidisciplinary
efforts leading to a greater understanding of homeostatic regulation.
Not only has the definition of “stress” been refined and updated based upon continued scientific
discoveries, but the perception of “stress” in domestic animals has evolved as well. Stress, as we
now know, includes indices such as environmental stress, nutritional stress, social stress, and
even prenatal stress. Animal stress is now identified as a unique event that elicits a specific
behavioral, physiological, neuroendocrine, endocrine, and/or immune response that may be as
unique as the stressful event itself.
The stress response is a complex and coordinated series of events initiated when stress sensors
in the brain stimulate the release of two neurohormones, corticotropin-releasing hormone (CRH)
and vasopressin (VP) in response to a stimulus. The parvocelular neurons within the
paraventricular nucleus (PVN) of the hypothalamus produce CRH, while magnocellular neurons
of the paraventricular and supraoptic nuclei are responsible for production of VP (Carrasco and
Van de Kar, 2003). Studies have indicated that some parvocellular neurons are capable of
producing both CRH and VP, suggesting a biological interaction between these two
neuropeptides. After traversing the blood vessels in the median eminence, CRH and VP can
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independently stimulate the production of adrenocorticotropic hormone (ACTH) from the
anterior pituitary (Aguilera, 1998; Carrasco and Van de Kar, 2003; Webster Marketon and
Galser, 2008). Subsequently, ACTH stimulates the production of glucocorticoids from the
cortex of the adrenal gland (Markara et al., 1981; Carrasco and Van de Kar, 2003). This
systematic cascade is often referred to as the hypothalamic-pituitary-adrenal (HPS) axis. In
mammals the primary glucocorticoid is cortisol. However, rodents lack the enzyme P450c17,
which is responsible for producing cortisol in the adrenal, and therefore their primary
glucocorticoid is corticosterone (Ashwell et al., 2000).
When released into the blood stream, cortisol can elicit a plethora of biological effects on the
body including changes in metabolism of carbohydrates and protein, alterations in the growth
and reproductive axes, regulation of the stress response, and influencing overall immune
function (Figure 1). Cortisol plays an important role in gluconeogenesis, the generation of
glucose from other organic molecules like pyruvate, lactate, glycerol, and amino acids, during
the “fight or flight” response. Cortisol increases blood glucose concentrations by stimulating the
liver to convert fat and protein to these intermediate metabolites that are ultimately converted to
glucose for energy (Long et al., 1940; McGuinness et al., 2005). Cortisol also supports the
primary defense response by enhancing the synthesis and secretion of catecholamines, other
stress hormones produced by the adrenal glands, which control physiological processes such as
heart rate, pupil dilation, vasoconstriction in the skin and gut, vasodilation in leg muscles, and
increased glucose production by the liver, all of which are essential processes during the “fight
or flight” response (Charmandari et al., 2005).
Figure 1. When an animal perceives either an internal or external threat, neurotransmitters are
released in the brain that cause the release of corticotrophin-releasing hormone (CRH) and
vasopressin (VP) which stimulate the release of adrenocorticotrophin (ACTH). ACTH in turn
stimulates the release of cortisol, epinephrine (Epi) and norepinephrine (NE), each of which
affects various target tissues in the body including the immune system.
Hypothalamus
Pituitary
Bone
Adipose
Muscle
Adrenals
Cortex
Medulla
ACTH
NE/Epi
Cortisol
STRESS
CRH/VP Visceral
Adiposity
Mass
Immune cells
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The sympathetic nervous system is activated in response to many stressors in parallel to and
often prior to the stimulation of the HPA axis. Upon stimulation, noradrenergic neurons in the
brain and postganglionic sympathetic neurons innervating peripheral organs (e.g., heart,
vasculature, kidneys, gut, and adipose) secrete norepinephrine into circulation, resulting in
increased blood pressure, heart rate, and respiration rate. Additionally, nerve impulses in high
cortical centers within the brain relay messages through the limbic system resulting in the
release of norepinephrine, serotonin, and acetylcholine, which activate the PVN (Black, 2002).
In conjunction with these actions, preganglionic sympathetic fibers innervating the adrenal
medulla stimulate the production and secretion of epinephrine and norepinephrine via
acetylcholine (Butcher and Lord, 2004).
The sympathetic nervous system regulates many functions in the body including cardiovascular,
gastrointestinal, respiratory, and renal systems, all of which can be modulated in response to
sympathomedulary system (SMS) activation (Charmandari et al., 2005). An increase in
epinephrine concentrations in the brain serves as an alarm system, resulting in a decrease in
neurovegetative activities (e.g., eating and sleeping) and the activation of the stress response
(HPA axis activation; Tsigos and Chrousos, 2002). The secretion of norepinephrine within the
brain also activates the fear behaviors and enhances long term memory and storage of adversely
charged emotions in the hippocampus (Salpolsky et al., 2000; Tsigos and Chrousos, 2002).
Additionally, the responses of the HPA axis and the SMS to stress are highly concordant. In
response to most stressors both systems are activated and have the ability to activate each other.
THE IMMUNE SYSTEM
The immune system is not a single entity, but rather a complex, integrated system regulated by a
multitude of specialized cells and chemical messengers. In general, however, the immune
system can be separated into three broad components; natural immunity, innate immunity, and
acquired immunity, all of which must be fully developed and functioning properly to provide
adequate immunological protection. Natural and innate immunity are typically grouped together
under the category of innate immunity. Therefore, when discussing innate immunity, it is
typically assumed that one is including natural immunity as well.
Innate immunity is considered to be the first line of defense against pathogens; whether
bacterial, viral, protozoal or fungal. It includes physical barriers such as the skin, mucosal
secretions, tears, urine, and stomach acid, as well as complement and antigen-nonspecific
cellular components and is designed to elicit an immediate or acute response (0 to 4 h) following
exposure to an antigenic agent (Männel, 2007; Barton, 2008). Until recently, the innate immune
system was thought to represent the antigen-nonspecific aspect of the immune system. However,
recent evidence suggests that the innate response may be specific to the pathogenic agent
encountered. While it is often assumed that this aspect of the immune system becomes a
constant entity once developed by the animal, this is certainly not the case. The innate immune
system, while always present to some degree, can be modulated in either a beneficial or
detrimental manner by a number of factors including wounds, dehydration, nutritional status,
genetics, stress, and various peptide hormones (Figure 2).
In response to inflammation, tissue damage, and infection, the body initiates an acute phase
response (APR). The APR is a set of reactions that promote tissue damage repair, control of
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invading organisms, would healing, and (or) recruitment of host defense mechanisms (Black,
2002). This includes the production of acute phase proteins from the liver, and production of
cytokines, catecholamines, and to a lesser extent, glucocorticoids. The APR is also characterized
by physiological responses within the animal including fever and sickness behavior (Black,
2002). This response usually subsides within 24 to 48 hours following stimulation.
Figure 2. Factors that can have a significant influence on the function of the innate immune
system of cattle. Naturally occurring deviations in the innate immune system as well as the
influence of various management practices on the immune system are often overlooked in
production systems.
STRESS EFFECTS ON IMMUNE FUNCTION
The immune system can be regulated by several different endocrine secretions, with the most
prominent being those secreted in response to stress. There has been an increased effort to
elucidate the interactions between stress responsiveness and immunological parameters in cattle
that may be either predisposed to or resistant to the detrimental effects of stress due to genetic
programming and/or prior experiences. Interestingly, there are cattle that demonstrate
differential stress and immunological responses due to previous exposure to various managerial,
environmental, nutritional, or pathogenic stressors or due to varying temperaments within a
genetically similar group of animals.
As researchers have continued to explore the complex interactions between stress and
production parameters such as growth, reproduction, and health, multidisciplinary efforts have
emerged that have led to a greater understanding of homeostatic regulation. Based upon these
efforts, our knowledge has extended beyond the "all or none" biological activity strictly
associated with the "fight or flight" response. For instance, researchers have demonstrated that
the combined immunological effects of cortisol and catecholamines result in a well-orchestrated
biological event designed to prevent over-stimulation of innate immunity and the production of
pro-inflammatory cytokines while simultaneously priming the humoral immune response in an
effort to provide adequate immunological protection (Sorrells and Salpolsky, 2007).
Genetic/Natural Deviations Management Influences
Breed Effects Diet Sexual Dimorphic Effects Housing Conditions Animal Temperament Effects Early vs Normal Weaning
Variations in Innate Immune Function
Stress Hormones
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Specifically, cortisol suppresses the release of various cytokines produced by cells of the
immune system which can cause systemic disease.
What is the purpose for inhibiting immune function in response to stress? First, it minimizes
potential autoimmune damage stemming from novel self-antigens that arise from catabolic
activity of glucocorticoids on immune cells and other tissues (Ráberg et al., 1998). Secondly, it
redirects resources to processes essential for survival such as heart rate, lung ventilation, and
other processes needed for escape or aggression (Sapolsky et al., 2000). In addition to
suppression of immune activity, there is catabolism of immune cells and other tissues in order to
increase availability of glucose and proteins for other body systems. However, suppressing the
immune system during acute stress would be counter intuitive for survival, and for a significant
energy savings to occur would require longer immune suppression (Martin, 2009).
Today, our knowledge base has expanded, and a greater appreciation and understanding has
emerged regarding the plethora of immune system activities that are influenced by cortisol such
as stimulation of immune system chemical messengers, and stimulation of immune cell growth
and function. In addition to these stimulatory actions, long-term exposure to cortisol is known to
inhibit aspects of immune function. Ultimately, within the animal, the immune system response
to stress is dependent upon the type of stress encountered (i.e., acute versus chronic). In some
instances of acute stress, such as that resulting from bites, punctures, scrapes or other challenges
to the integrity of the body, stress hormones are associated with priming the immune system in a
manner to prepare for potentially invading pathogens and subsequent infection. However, when
an animal experiences prolonged or “chronic” stress, the effect of stress hormones on the
immune system shifts from a preparatory event to a series of suppressive events first at the
cellular level and then eventually across the entire immune system spectrum. Several factors
influence the stress-immune interaction, including age, breed/species, environment, gender,
health status, previous exposure, and personality/temperament.
Acute Stress
While is has been known for decades that “stress” can have detrimental effects on the immune
system, it was only recently that the divergent effects of “acute” stress compared to long-term or
“chronic” stress were revealed. As the scope of scientific exploration beyond traditionally
defined pathways of neuroendocrinology, endocrinology, and immunology, multidisciplinary
efforts emerged, cross-communication pathways among the stress and immune systems have
emerged, and have lead to a better understanding of homeostatic regulation within the animal.
No longer is stress considered strictly immunosuppressive. Indeed, stress may elicit “bi-
directional” effects on immune function such that acute stress may be immunoenhancing, while
chronic stress may be immunosuppressive.
Acute stress is stress that occurs for a short period of time – typically seconds or minutes. While
chronic stress, discussed below, has typically been associated with negative effects on immune
function, acute stress has been demonstrated to have a priming effect on the immune system.
Specifically, studies have demonstrated an increase in maturation and trafficking of immune
cells (i.e., neutrophils and natural killer cells) to the periphery and target tissues, up-regulation
of several cytokines and chemokines, enhanced response to vaccination and an enhanced
response to a second pathogen exposure (Dhabhar, 2000; Dhabhar, 2002; Dhabhar et al., 2009).
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Stress hormones, particularly glucocorticoids produced by the adrenal gland, are necessary for
the development of the thymus, as adrenal insufficiency or adrenalectomy results in hypertrophy
of the thymus that is not reversed by epinephrine administration (Ashwell et al., 2000).
Additionally, the ability to respond to glucocorticoids though the glucocorticoid receptor (GR)
is necessary for the development of T cells in the thymus, as inhibition of the GR limits the
production of mature T cells (Bellinger et al., 2008). Stress hormones are responsible for
increases in cholesterol, lipoproteins, triglycerides and free fatty acids, which may be beneficial
during the stages of early infections as lipoproteins can bind and thereby neutralize
lipopolysaccharide (LPS; component of the cell wall of gram negative bacteria; Black, 2002).
Studies have also demonstrated that cortisol administered 144 hour or less prior to an endotoxin
(LPS) challenge can enhance the cytokine response, perhaps by priming the immune system
(Besedovsky et al., 1996; Sapolsky et al., 2000; Sorrells and Sapolsky, 2007). In contrast,
glucocorticoid administered at the same time or after the administration of endotoxin suppresses
these responses (Sapolsky et al., 2000). Additionally, in a review by Sorrells and Sapolsky
(2007), the authors stated that the early response to invading pathogens is characterized by low
concentrations of glucocorticoids that are permissive; later responses to pathogens,
characterized by high concentrations of glucocorticoids, results in the negative effects on
immune function. Therefore, the timing relative to immune system activation is extremely
important in determining whether stress hormones will have stimulatory and inhibitory effects
on the immune system.
A study in which ACTH was administered to Brahman heifers reported an increase in the
expression of interleukin-10 (IL-10), interferon-γ (IFN-γ), IL-4, tumor necrosis factor- α (TNF-
α), and the GR in isolated peripheral blood mononuclear cells (PBMCs; Burdick et al., 2010).
This suggested that acute ACTH-induced increases in cortisol can modulate cytokine and GR
gene expression, potentially resulting in a priming effect on the immune system. Administration
of short-acting dexamethasone to Hereford steers, mimicking in vivo increases in cortisol,
resulted in an increase in many immune cells and immune cell function parameters, which also
supports the conclusion that acute stress can prime the immune system for subsequent responses
(Anderson et al., 1999). Acute stress induced by weaning has also been reported to influence
immune cell numbers as well as cytokine gene expression in calves. Specifically, expression of
IL-β, toll-like receptor 4 (TLR4), and GRα by leukocytes were increased in response to weaning
(O’Loughlin et al., 2011). However, while weaning alone may result in an acute stressor,
weaning is typically accompanied by transportation and the addition of novel management
practices and handling, which may heighten the exposure to stress resulting in chronic stressor
exposure.
Chronic Stress
In contrast to acute stress, chronic stress is stress that is either repeated or exerted for an
extended period of time – typically hours to days, weeks, months, or longer. Chronic stress has
been associated with delayed wound healing, enhanced immunosuppressive actions, increased
changes for development of autoimmune and inflammatory diseases and cancer, reduced
cytokine responsiveness of natural killer cells, reduced mucosal immunity, and decreased ability
of lymphocytes to proliferate, respond to pathogens, and release immunoglobulins (McEwen et
al., 1997; Ashwell et al., 2000; Sapolsky et al., 2000; Silberman et al., 2003).
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Chronic exposure to high concentrations of cortisol can cause severe physiological and
psychological problems such as excessive protein catabolism, hyperglycemia,
immunosuppression, and depression (McEwen et al., 1997). In domestic livestock, excessive
concentrations of cortisol have been linked to reduced rates of reproduction, suboptimal growth,
suppressed milk production, and suppression of immune function that could increase
susceptibility to disease (Moberg, 1987; Dobson et al., 2001; Silberman et al., 2003; Zhao et al.,
2008). Additionally, glucocorticoids can modulate the expression of cytokines and their
receptors, including pro-inflammatory TNF-α (Ashwell et al., 2000). Corticosteroids have been
noted to decrease the secretion of IL-1β, IL-2, IL-6 and IFN-γ and increase receptors for IFN-γ,
IL-1β, IL-6, VP, CRH, serotonin, and insulin (Black, 2002).
In livestock, administration of dexamethasone to Holstein steers induced neutrophilia, or an
increase in circulating neutrophils, while reducing the expression of L-selectin, an adhesion
molecule that allows neutrophils to extravasate into tissues (Weber et al., 2004). Glucocorticoids
also increase the half-life of neutrophils. This can result in excessive damage to healthy tissue
due to their longer life and the extended time in which neutrophils can produce cytotoxic
granules (McEwen et al., 1997). Interestingly, neutrophils can release specific proteases that
cleave glucocorticoids from cortisol binding globulin, therefore increasing the amount of “free”
cortisol within tissues (McEwen et al., 1997). There is also evidence that stress hormones can
affect the maintenance of the memory cell pool (Burns et al., 2003).
In neonatal Holstein bull calves administered dexamethasone twice daily from 3 to 56 days of
age, expression of TLR2, TLR4 and IL-1 were reduced in blood leukocytes, suggesting chronic
administration of dexamethasone inhibited the recognition of pathogens in young calves (Eicher
et al., 2004). Additionally, a study in Angus and Romosinuano heifers exposed to heat stress for
2 weeks reported a diminished cortisol response and an altered immune response to subsequent
LPS challenge, suggesting that chronic heat stress down-regulated immune responsiveness
(Burdick et al., 2012). Therefore, chronic stress may prevent cattle from recognizing and
eliciting an adequate immune response to an invading pathogen.
CONCLUSION
Ultimately, the combined immunological effects of cortisol and catecholamines result in a well-
orchestrated event designed to prevent over-stimulation of innate immunity while
simultaneously priming the acquired immune response. Therefore, the final type of immune
response that prevails within an animal is dependent upon the overall type and duration of the
stress response in the animal.
Given that the innate immune system provides the first line of defense, understanding the effects
of stress hormones on innate immunity holds a great deal of potential with regard to improving
cattle health, and ultimately productivity. Continued research efforts into these complex
interactions may allow the implementation of alternative management practices, improved
selection programs, and/or implementation of various nutritional strategies to prevent or
overcome significant production losses and animal health care costs for livestock producers.
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Dhabhar, F.S. 2009. Enhancing versus suppressive effects of stress on immune function:
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Makara, G.B., E. Stark, M. Karteszi, M. Paklovits, and G. Rappay. 1981. Effects of
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2004. Mechanisms of glucocorticoid-induced down-regulation of neutrophil L-selectin
in cattle: evidence for effects at the gene-expression level and primarily on blood
neutrophils. J. Leukoc. Biol. 75:815-827.
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Predicting Transition Cow Health and Performance – Use of Blood and
Fecal Biomarkers for Herd-Level Evaluation and Diagnostics
J. M. Huzzey
1,†, D. V. Nydam
2, P. A. Ospina
1, and T. R. Overton
1
1 Department of Animal Science
2 Department of Population Medicine and Diagnostic Sciences
Cornell University, Ithaca NY
Corresponding author: [email protected]
SUMMARY
Nonesterified fatty acids and beta-hydroxybutyrate in plasma are indices of energy
metabolism in transition cows and can be used to assess opportunities for improved health,
performance, and reproduction
Plasma haptoglobin is a nonspecific indicator of inflammation and acute phase response
and is associated with decreased subsequent milk production and reproductive performance
Fecal cortisol metabolites can also be used as a nonspecific biomarker of stress in transition
dairy cows, and its most meaningful associations are with milk yield and reproductive
performance rather than clinical disease
INTRODUCTION
Blood metabolites have been used in herd-level diagnostics of transition cow management for a
number of years (Ingraham and Kappel, 1988; Herdt, 2000; Oetzel, 2004), mostly with focus on
identifying opportunities to decrease the incidence of metabolic disorders related to energy
metabolism. Recently, there has been a resurgence of interest in the use of blood metabolites,
primarily nonesterified fatty acids (NEFA) and beta-hydroxybutyrate (BHBA) for evaluation of
transition cow programs. This resurgence is largely based on recent findings that both NEFA
and BHBA are associated with economically important herd parameters beyond metabolic
disease incidence, namely milk production and reproductive performance. In addition, the
increased availability of accurate cow-side tests for BHBA in blood (Precision Xtra, Abbott
Laboratories) and milk (KetoTest, Elanco Animal Health) has made routine evaluation of
BHBA in herds simple, fast, and low cost. In light of these findings, new research has begun to
evaluate the relationships of biomarkers related to stress and inflammation [e.g. plasma
haptoglobin (Hp) and fecal cortisol metabolites (FCORT)] with metabolic disease, milk
production, and reproduction in order to identify other useful and physiologically relevant
markers for herd-level diagnostics and evaluation of transition cow programs. This paper
reviews our recent findings in these areas and provides recommendations on how these markers
should be interpreted for evaluating transition cow programs.
USE OF ANALYTES RELATED TO ENERGY METABOLISM – NEFA & BHBA
Oetzel (2004) characterized well the typical use of blood analytes related to energy metabolism
in transition management diagnostics – NEFA during the prepartum period to assess precalving
energy status and BHBA during the postpartum period to assess incidence of subclinical (and
† Current affiliation: Animal Welfare Program, University of British Columbia, Vancouver BC
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clinical) ketosis. This approach was supported in part by work conducted in Michigan
(Cameron et al., 1998) that associated increased prepartum concentrations of NEFA, reflective
of negative energy balance, with a greater incidence of displaced abomasum. Duffield et al.
(1998) defined and characterized subclinical ketosis in herds in Ontario during the postpartum
period and demonstrated that administration of monensin in a controlled-release capsule would
decrease the incidence of subclinical ketosis in dairy cows during early lactation.
Recently, our group conducted a large-scale evaluation of the associations of prepartum NEFA
and postpartum NEFA and BHBA with postpartum health, milk production, and reproductive
performance in dairy herds in the northeastern US (Ospina et al., 2010a, 2010b, 2010c). In order
to have been included in the study a herd must have: 1) had greater than 250 milking cows, 2)
housed cows in free-stalls, 3) fed a total mixed ration (TMR), and 4) participated in DHIA
and/or use Dairy Comp 305 (Valley Ag. Software, Tulare CA). Farms were visited once and
during the farm visit two cohorts of animals were selected: those 14 to 2 days prepartum and
those 3 to 14 days postpartum. Within each cohort, convenience samples of 15 apparently
healthy animals were evaluated. Briefly, 10 mL of blood was collected from the coccygeal vein
or artery into a red-top tube. The sera from the prepartum cohort were analyzed for NEFA and
the sera from animals sampled after calving were analyzed for NEFA, BHBA. For all animals
sampled, the incidence of the diseases of interest [displaced abomasum (DA), clinical ketosis
(CK), and metritis (MET) and/or retained placenta (RP)] within 30 days in milk, time to
pregnancy within 70 days post voluntary waiting period and Mature Equivalent 305 (ME 305)
milk at 120 days in milk were recorded. The final dataset included 100 herds with an average
herd size of 840 cows. A total of 2758 cows were sampled within these herds (1440 animals
sampled prepartum and 1318 sampled postpartum) with an approximate distribution of 35%
primiparous (entering first lactation) and 65% multiparous (entering second or greater lactation)
cows.
Critical threshold values for prepartum NEFA and postpartum NEFA and BHBA and the
associated risk ratios for disease are presented in Table 1. If animals had prepartum serum
NEFA concentrations greater than about 0.30 mEq/L, they were twice as likely to develop one
or more of the diseases of interest. Animals with postpartum serum NEFA and BHBA
concentrations greater than about 0.60 mEq/L and 10 mg/dL, respectively, were four times as
likely to develop one of more of the diseases of interest than animals with lower concentrations
of these metabolites. The risk ratio for individual disorders varied widely within these groups.
These results are consistent with prior work and support the importance of maintaining adequate
energy intake prepartum and controlling body condition score loss and overall energy status
during the postpartum period with respect to disease.
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Table 1. Receiver operator characteristic (ROC) curve determination of critical NEFA (mEq/L)
and BHBA (mg/dL) thresholds as predictors of disease and risk ratios of disease based upon these
critical thresholds (Ospina et al., 2010b).
Prepartum cohort (2 to 14 days prepartum)
Disease Critical prepartum
NEFA1
Risk
Ratio
95 % CI2 P-value
DA 0.27 2.0 1.1 – 3.7 0.03
CK 0.26 1.8 1.2 – 2.5 0.001
Met and/or RP 0.37 2.2 1.6 – 3.0 < 0.0001
Any of the three 0.29 1.8 1.4 – 2.2 < 0.0001
Postpartum cohort (3 to 14 days postcalving)
Disease Critical postpartum
NEFA1
Risk
Ratio
95 % CI2 P-value
DA 0.72 9.7 4.2 – 22 <0.0001
CK 0.57 5.0 2.3 – 11 <0.0001
Met 0.36 17 2.0 – 134 0.008
Any of the three 0.57 4.4 2.6 – 7.3 < 0.0001
Disease Critical BHBA1 Risk
Ratio
95 % CI2 P-value
DA 10 6.9 3.7 – 12.9 <0.0001
CK 10 4.9 3.2 – 7.3 <0.0001
Met 7 2.3 1.1 – 5.1 0.037
Any of the three 10 4.4 3.1 – 6.3 <0.0001 1 Highest combination of specificity and sensitivity based upon ROC analysis
2 Risk ratio confidence interval
The relationships of prepartum NEFA and postpartum NEFA and BHBA with reproductive
performance for the first 70 days after voluntary waiting period are described in Table 2.
Animals with prepartum NEFA greater than about 0.3 mEq/L were nearly 20% less likely to
become pregnant than animals with lower concentrations. Animals with greater than about 0.70
mEq/L of NEFA (while controlling for BHBA) and/or greater than 10 mg/dL of BHBA were 13
to 16% less likely to become pregnant than animals with lower concentrations. In all models,
multiparous cows were less likely than primiparous cows to become pregnant in the first 70
days following the voluntary waiting period.
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48
Table 2. Cox proportional hazard model of the effect of NEFA (mEq/L) and/or BHBA (mg/dL),
covariates, and animals clustered within herds on days to conception after voluntary waiting
period (Ospina et al., 2010a).
Sampled population Variable Hazard P-value
Prepartum cohort NEFA ≥ 0.27
Parity
0.81
0.73
0.01
0.001
Postpartum cohort NEFA ≥ 0.72
BHBA ≥ 10
Parity
0.84
0.93
0.81
0.05
0.4
0.01
Postpartum cohort BHBA ≥ 10
Parity
0.87
0.80
0.1
0.01
Associations of analytes related to energy metabolism with subsequent milk production
(assessed as mature-equivalent 305-day lactational milk, predicted at approximately 120 DIM)
are depicted in Table 3. Regardless of parity, animals with greater than about 0.3 mEq/L of
NEFA during the prepartum period had nearly 700 kg less ME305 projected milk than animals
with lower concentrations. During the postpartum period, there were interesting differences in
associations of energy-related analytes with milk production depending upon parity. In
primiparous cows (heifers), postpartum NEFA concentrations greater than about 0.6 mEq/L and
BHBA concentrations over about 9 mg/dL were associated with increased milk yield. In
multiparous cows, postpartum NEFA concentrations greater than about 0.7 mEq/L and BHBA
concentrations greater than about 10 mg/dL were associated with lower predicted milk yield.
Table 3. Mixed models for the effect of NEFA (mEq/L) and/or BHBA (mg/dL), covariates, and
herd as a random effect on milk production assessed as ME305 milk at 120 days in milk (Ospina
et al., 2010a).
Sampled Population Variable Difference in ME milk yield (kg) P-value
Prepartum NEFA ≥ 0.33
Parity
-683
-556
0.001
0.01
Postpartum -- heifers NEFA ≥ 0.57
BHBA ≥ 10
+488
-143
0.02
0.5
Postpartum -- heifers BHBA ≥ 9 + 403 0.04
Postpartum -- cows NEFA ≥ 0.72
BHBA ≥ 10
-647
-165
0.001
0.4
Post-partum -- cows BHBA ≥ 10 -393 0.04
Among animals sampled during the prepartum period (2 to 14 days before calving), 45% of
primiparous animals and 26% of multiparous cows had NEFA concentrations at or above 0.3
mEq/L. Among animals sampled during the postpartum period (3 to 14 days after calving), 25%
of primiparous animals and 33% of multiparous cows had NEFA concentrations at or above 0.7
mEq/L. Furthermore, 15% of primiparous animals and 27% of multiparous cows had BHBA
concentrations at or above 10 mg/dL. In the vast majority of participating farms, primiparous
and multiparous animals would have been commingled during the period before calving– these
results suggest that heifers in particular may be compromised from the standpoint of energy
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49
intake relative to requirements in these systems. Furthermore, these energy-related analytes
appear more likely to be elevated in multiparous cows than primiparous cows during the period
after calving.
Ospina et al. (2010c) also used this dataset to compare herds with greater than 15% of animals
over the critical thresholds for the analytes during the prepartum and postpartum periods with
those with less than 15% of animals over the thresholds during each period and results from this
analysis are presented in Table 4. It should be noted that the numbers in this table reflect the
associations among all animals in the herd, not just sampled animals in the study. As suggested
by the results in the table, those herds with more than 15% of animals with prepartum NEFA
and/or postpartum NEFA and BHBA over the critical thresholds had slightly greater disease
incidence, poorer reproductive performance, and lower ME305 projected milk yield in both
primiparous and multiparous cows. In the U.S. system, the associations of these analytes at the
herd-level with decreased milk yield and poorer reproductive performance would be much more
economically meaningful than those with disease incidence.
Table 4. Herd-level impacts of elevated prepartum and postpartum nonesterified fatty acids
(NEFA) and postpartum beta-hydroxybutyrate (BHBA) in commercial dairy farms (Ospina et al.,
2010c)
Metabolite level Herd alarm Herd-level impact
Prepartum NEFA (14 to 2 d prepartum)
> 0.3 mEq/L
> 15% - 1.2% 21-d pregnancy rate
+ 3.6% disease incidence
- 282 kg ME305 milk
Postpartum NEFA (3 to 14 d postpartum)
> 0.6 (heifers) – 0.7 (cows) mEq/L
> 15% - 0.9% 21-d pregnancy rate
+ 1.7% disease incidence
Heifers: - 288 kg ME305 milk
Cows: -593 kg ME 305 milk
Postpartum BHBA (3 to 14 d postpartum)
> 10 (cows) – 12 (heifers) mg/dL
> 15%
> 20%*
- 0.8% 21-d pregnancy rate
+ 1.8% disease incidence
*Heifers: -534 kg ME305 milk
Cows: -358 kg ME 305 milk
15% of 15 animals sampled = 2 to 3 animals over threshold; 90% confidence interval that it
sample represents herd prevalence
In terms of practical application of this information, we believe that measurement of energy-
related analytes is a useful tool for monitoring herds, evaluation of potential opportunities for
improved transition cow management, or diagnostics. In terms of the target windows, we
recommend sampling 12 to 15 cows per group within the windows of interest described above –
prepartum samples should be analyzed for NEFA and postpartum samples can be analyzed for
NEFA and/or BHBA. The cowside blood or milk tests for BHBA described above are very
accurate and represent an excellent first step or front line analysis because of convenience and
cost. Because the incidence of herds with high postpartum NEFA in our dataset was much
greater than that with high postpartum BHBA, we would encourage practitioners and
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50
consultants to take the extra step and consider analysis for postpartum NEFA in situations where
they believe that early lactation milk production and reproductive performance are compromised
yet the BHBA data are unrevealing. Finally, prepartum NEFA continue to be useful in helping
to identify situations in which larger than desired proportions of prepartum cows have
compromised energy status.
Table 5 describes three possible outcomes and potential interpretations for a herd to consider
after NEFA and/or BHBA evaluation in prepartum and postpartum groups. If NEFA is elevated
in prepartum cows, it is generally a good signal that either energy intake as a whole is
inadequate or facility/management issues exist and are causing significant cow to cow variation
in DMI and hence NEFA concentration. Independent of postpartum analyte values, we associate
elevated prepartum NEFA with negative disease, reproductive, and production outcomes at the
herd level (Table 4). The most likely analyte pattern for a herd that is overfeeding energy either
far-off or close-up is low NEFA values prepartum but high NEFA and/or BHB values
postpartum. Herds and consultants should remember, however, that a number of factors specific
to either nutritional management or facility/grouping management also can elevate postpartum
concentrations of NEFA and/or BHB independent of prepartum values. Typically, when herds
are overfed either far-off or close-up, we see a subsequent rapid and marked loss of BCS among
fresh cows – NEFA testing of the fresh cows can help to confirm this.
Table 5. Interpretation of energy-related metabolites [nonesterified fatty acids (NEFA) and
beta-hydroxybutyrate (BHBA)] to assess herd-level opportunities.
Scenario Likely cause and possibilities
High prepartum NEFA
High postpartum NEFA and/or BHBA
Likely starting with low DMI in close-up cows
Too low energy in prefresh diet, facility and/or
management issues (grouping, stocking density, heat
stress?)
High prepartum NEFA
Low postpartum NEFA and/or BHBA
Low DMI in close-up cows
Sampling the survivors in the fresh pen?
Is herd outmanaging or putting band-aids on fresh cow
issues?
Low prepartum NEFA
High postpartum NEFA and/or BHBA
Is herd overfeeding energy either far-off or close-up?
Diet or facility/management issues specific to
maternity/fresh group
POTENTIAL FIELD-BASED MARKERS FOR INFLAMMATION AND STRESS IN
TRANSITION COWS
An emerging area of focus within our research group is in understanding the relationship of
inflammation and stress with transition cow health and performance (Huzzey et al., 2011;
Huzzey and Overton, 2010). We envision that biomarkers related to inflammation [e.g.
Haptoglobin (hp)] or stress [fecal cortisol metabolites (FCORT)] could also be useful for
evaluating the effects of non-nutritional management factors, such as overstocking or
commingling of cows and heifers, on physiology. Haptoglobin is an acute phase protein that is
synthesized and released by liver as part of the inflammatory response and has been shown to be
elevated in cows with metritis (Huzzey et al., 2009). Although there are many acute phase
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51
proteins, Hp has been of particular interest for the detection of sick animals due to its very low
concentrations in the blood of healthy animals (Eckersall, 2000). Fecal cortisol metabolites are
reflective of circulating concentrations of cortisol approximately 10 to 12 hours prior to the
collection of the fresh fecal sample. Concentrations of FCORT have been suggested to be a
better indictor of physiological stress responses than direct measurements of plasma cortisol due
to the feedback-free nature of the sampling method (Palme et al., 1999). Restraint and handling,
which are required during blood sampling, can cause a physiological stress response and raise
circulating cortisol concentrations quickly (Cook et al., 2000). Further, the release of cortisol
from the adrenal gland during the day is pulsatile and has a diurnal cycle that is subject to
substantial individual variation. Because FCORT does not have the same limitations relative to
sampling, as does serum or plasma cortisol, it offers a potential way to study activation of the
hypothalamic-pituitary-axis in response to exposure to stressors.
To evaluate whether prepartum physiological indicators of stress and inflammation were
associated with the occurrence of health disorders after calving and milk yield, data were
collected from 412 cows on two commercial dairies in New York State. Farms were visited
weekly to collect blood, fecal samples, and BCS. Sampling began approximately 4 wk prior to
each cow’s expected calving date. One blood and fecal sample per cow was collected between d
-21 to -15 relative to the actual calving date to represent wk -3, d -14 to -8 (wk -2), and d -7 to -
2 (wk -1). Prepartum plasma was analyzed for NEFA, Hp, and cortisol and FCORT
concentrations (11,17-dioxoandrostanes) were determined from fecal samples.
Health events occurring within 30 DIM, including retained placenta (RP), displaced abomasum
(DA), and death (not including voluntary culls) were collected from DairyCOMP 305. A
postpartum blood sample was collected within 3 to 10 d after calving. Based on this postpartum
blood sample, sub-clinical ketosis (SCK) was diagnosed when plasma BHBA was ≥ 10 mg/dl
(Ospina et al., 2010a) and High Haptoglobin (HiHp, suggestive of an infection such as metritis)
was diagnosed when plasma Hp was ≥ 1 g/L (Huzzey et al., 2009). Cows were divided into 3
health categories for statistical analysis: 1) No disorder of interest (NDI); 2) One disorder (RP,
DA, SCK, or HiHp); or 3) More than one disorder (RP, DA, SCK, HiHp) or death.
As expected prepartum plasma NEFA was a strong predictor of postpartum health; however,
this relationship was dependent on the degree of illness after calving. Cows that developed
multiple disorders after calving or that died had the greatest concentrations of NEFA, relative to
the other two health categories, particularly during the 2-week period before calving. There
were no associations between prepartum Hp or FCORT concentration and the occurrence of one
disorder (RP, DA, SCK or HiHP) by 30 DIM. Hp concentration tended to be greater during wk -
2 and -1 and FCORT tended to be greater during wk -3 and -2 for cows that developed more
than one disorder or that died by 30 DIM relative to cows the NDI category; however, neither of
these analytes could predict which cows would go on to develop health complications as well as
prepartum NEFA concentration (Huzzey et al., 2011).
In order to evaluate the relationships of these analytes with subsequent milk yield, herd DC305
records were used to collect information on each cows predicted 305ME from the 2nd
test day
(approximately 62 DIM). A range of metabolic cutpoints were evaluated for each period and the
effect of being above or below the cutpoint on predicted 305ME was then evaluated (Huzzey
and Overton, 2010).
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1176
-257
-863-999
-2275
-2583
-1041
-2926
-3500
-3000
-2500
-2000
-1500
-1000
-500
0
500
1000
1500
Diffe
ren
ce
* in
30
5M
E M
ilk Y
ield
(lb
s)
primiparous
multiparous
* Dif f erence = (305MP cows abov e cutpoint) - (305ME cows below cutpoint)
wk -3 wk -2 wk -1 wk +1
FCORT Cutpoints: > 2500 ng/g fecal DM > 700 ng/g fecal DM
***
***
Projected 305ME milk yield tended to be 2328 lbs lower in heifers with haptoglobin
concentrations > 1.1 g/L during weeks -3 and -2, relative to heifer below this cutpoint.
Multiparous cows with haptoglobin > 1.1 g/L during weeks -2, -1 or +1 had on average 3315 lbs
lower projected 305ME milk yield (Figure 1), relative to multiparous cows below this cutpoint.
Figure 1. Difference in predicted 305ME milk yield for cows above the indicated Haptoglobin
(Hp) cutpoints relative to cows that are below the cutpoints
There was no association between plasma cortisol and milk yield at any period relative to
calving for either multiparous or primiparous cows (data not shown). Concentrations of FCORT
were not significantly associated with 305ME milk yield in primiparous cows; however,
multiparous cows with FCORT > 2500 ng/g fecal DM during weeks -3 or -2 relative to calving
had on average 2429 lbs lower 305ME milk yield relative to cows below this cutpoint. Projected
305ME milk yield was 2926 lbs lower among MP cows with fecal cortisol metabolites > 700
ng/g fecal DM during week +1 (Figure 2).
Figure 2. Difference in predicted 305ME milk yield for cows above the indicated fecal cortisol
metabolite (FCORT) cutpoints relative to cows that are below the cutpoints
-2654
-2002-2224
-721
-1634
-2315
-5130
-2500
-6000
-5000
-4000
-3000
-2000
-1000
0
Diffe
ren
ce
* in
30
5M
E M
ilk Y
ield
(lb
s)
primiparous
multiparous
* Dif f erence = (305MP cows abov e cutpoint) - (305ME cows below cutpoint)
wk -3 wk -2 wk -1 wk +1
Hp Cutpoint: > 1.1 g/L
*
**
***
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In summary, cows with higher concentrations of NEFA (data not shown; with the exception of
heifers during week +1), haptoglobin, or fecal cortisol metabolites around calving have lower
projected 305ME at the 2nd
test day and these associations are apparent up to 3 weeks prior to
the onset of lactation. While higher concentrations of NEFA, Hp, and FCORT are associated
with lower predicted milk yield, the significance of these relationships was stronger for Hp and
FCORT relative to NEFA, particularly when these analytes are measured during the week after
calving. If we focus on the postpartum period it is also appears that both Hp and FCORT are
more sensitive to 305ME milk yield projections than NEFA; the magnitude of the difference in
projected 305ME between those animals that were above versus below the indicated cutpoints
were much greater when using Hp or FCORT to predict these differences compared to NEFA.
Finally, a greater proportion of animals were above the Hp and FCORT cutpoints during week
+1 then were above the NEFA cutpoint. These results suggest that haptoglobin or fecal cortisol
metabolites may be alternative and perhaps more effective analytes for detecting cows at risk for
reduced milk yield, than NEFA.
Associations of postpartum concentrations of NEFA and Hp with reproductive performance as
assessed using Kaplan-Meier analysis are shown in Figure 3. Consistent with previous work,
cows with elevated concentrations of NEFA postcalving had longer times to pregnancy.
Similarly, cows with elevated concentrations of Hp had longer times to pregnancy.
Collectively, these results suggest that both compromised energy balance and inflammation
have strongly negative associations with subsequent reproductive performance.
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54
Figure 3. Graph of Kaplan-Meier estimator of days to conception for primiparous cows with
postpartum (3 to 10 DIM) nonesterified fatty acid (NEFA; A) concentrations > or ≤ 0.45 mEq/L
(P = 0.02) and postpartum haptoglobin (Hp; B) concentrations > or ≤ 1.3 g/L (P = 0.02).
SUMMARY AND CONCLUSIONS
Circulating concentrations of energy-related metabolites (prepartum NEFA and postpartum
NEFA and/or BHBA) are highly associated with postpartum outcomes relative to disease, milk
production, and reproductive performance in dairy cattle. As such, they can be an important
component of evaluation of transition cow programs. Our recent data suggest that associations
of elevated concentrations of these metabolites during the prepartum and postpartum period with
subsequent milk yield and reproductive performance may be more meaningful at the farm level
than their associations with metabolic disease. Because of convenience and cost, evaluation of
Days in Milk
0
10
20
30
40
50
60
70
80
90
100
0 30 60 90 120 150
Hp < 1.3 g/L Postpartum
Hp > 1.3 g/L Postpartum
B
Pri
mip
arous
Cow
s not
Pre
gnan
t
(%)
0
10
20
30
40
50
60
70
80
90
100
0 30 60 90 120 150
NEFA < 0.45 mEq/L Postpartum
NEFA > 0.45 mEq/L Postpartum
A
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postpartum BHBA in milk or blood at the farm level is a preferred first-line monitoring tool,
although prepartum and postpartum NEFA concentrations in serum or plasma can provide
additional insight into transition management opportunities. New research from our group
suggests that elevated concentrations of biomarkers related to inflammation and stress (plasma
haptoglobin and fecal cortisol metabolites) during the transition period also are associated with
decreased milk yield and reproductive performance in early lactation – we will be conducting
further research to develop these as potential tools to help identify opportunities for improved
transition cow management.
REFERENCES
Cameron, R. E., P. B. Dyk, T. H. Herdt, J. B. Kaneene, R. Miller, H. F. Bucholtz, J. S. Liesman,
M. J. VandeHaar, and R. S. Emery. 1998. Dry cow diet, management, and energy balance
as risk factors for displaced abomasums in high producing dairy herds. J. Dairy Sci. 81:132-
139.
Cook, C.J., D. J. Mellor, P. J. Harris, J. R. Ingram, and L. R. Matthews. 2000. Hands-on and
hands-off measurement of stress. In: Moberg G.P. and J. A. Mench, ed. The Biology of
Animal Stress. CABI Publishing, p.123-46.
Duffield, T. F., D. Sandals, K. E. Leslie, K. Lissemore, B. W. McBride, J. H. Lumsden, P. Dick,
and R. Bagg. 1998. Efficacy of monensin for the prevention of subclinical ketosis in
lactating dairy cows. J. Dairy Sci. 81:2866-2873.
Eckersall, P. D. 2000. Recent advances and future prospects for the use of acute phase proteins
as markers of disease in animals. Rev. Med. Vet. 151:577-584.
Herdt, T. H. 2000. Variability characteristics and test selection in herd-level nutritional and
metabolic profile testing. Vet. Clin. North Am. Food Anim. Pract. 16:387-403.
Huzzey, J. M., T. F. Duffield, S. J. LeBlanc, D. M. Veira, D. M. Weary, and M. A. von
Keyserlingk. 2009. Short communication: Haptoglobin as an early indicator of metritis. J.
Dairy Sci. 92:621-625.
Huzzey, J. M., and T. R. Overton. 2010. Measuring the effect of stress during the transition
period on subsequent health and performance of dairy cattle. Proceedings, Cornell Nutrition
Conference for Feed Manufacturers, Syracuse, NY, pp. 76-86. Accessed on 6/1/2011 at
http://www.ansci.cornell.edu/cnconf/2010proceedings/index.html
Huzzey J. M., D. V. Nydam, R. J. Grant, and T. R. Overton. 2011. Associations of prepartum
plasma cortisol, haptoglobin, fecal cortisol metabolites, and nonesterified fatty acids with
postpartum health status in Holstein dairy cows. J. Dairy Sci. 94 :5878–5889.
Ingraham, R. H., and L. C. Kappel. 1988. Metabolic profile testing. Vet. Clin. North Am.
Food Anim. Pract. 4:391-411.
Oetzel, G. R. 2004. Monitoring and testing dairy herds for metabolic disease. Vet. Clin. North
Am. Food Anim. Pract. 20:651-674.
Ospina, P. A., D. V. Nydam, T. Stokol, and T. R. Overton. 2010a. Associations of elevated
nonesterified fatty acids and beta-hydroxybutyrate concentrations with early lactation
reproductive performance and milk production in transition dairy cattle in the northeastern
United States. J. Dairy Sci. 93:1596-1603.
Ospina, P. A., D. V. Nydam, T. Stokol, and T. R. Overton. 2010b. Evaluation of nonesterified
fatty acids and beta-hydroxybutyrate in transition dairy cattle in the northeastern United
States: Critical thresholds for prediction of clinical diseases. J. Dairy Sci. 93:546-54.
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Ospina, P. A., D. V. Nydam, T. Stokol, and T. R. Overton. 2010c. Association between the
proportion of sampled transition cows with increased nonesterified fatty acids and β-
hydroxybutyrate and disease incidence, pregnancy rate, and milk production at the herd
level. J. Dairy Sci. 93:3595-3601.
Palme, R., C. Robia, S. Messmann, J. Hofer, and E. Möstl. 1999. Measurement of faecal cortisol
metabolites in ruminants: a non-invasive parameter of adrenocortical function. Wien.
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57
Economics of Feeds in Dairy Rations
N. R. St-Pierre and W. P. Weiss
Department of Animal Sciences
The Ohio State University, Columbus, OH-43210
Corresponding author: [email protected]
SUMMARY
The economic value of a feed rests in the value of its nutrients. In dairy, the economically
important nutrients are net energy lactation (NEL), metabolizable protein (MP), effective
NDF (eNDF), and non-effective NDF (neNDF).
Unit prices of the important nutrients can be calculated using the composition and prices of
all feeds being traded in a given market. This method is available in a Windows-based
software. Alternatively, estimates of unit prices are being published on a monthly basis in a
national dairy magazine for all major dairy regions.
Forage composition for NEL, MP, eNDF and neNDF can easily be determined using 11
compositional inputs and equations provided in the appendix of this paper. Using data from
our experimental research station, we do not find a strong association between in vivo total
tract NDF digestibility and in vitro NDF digestibility (NDFd). At this point we are still
recommending the use of protein-free NDF and lignin to estimate NDF digestibility.
For most feeds, the economic value is calculated as the simple sum of the values of their
nutrients. With forages, however, one must introduce a correction associated with quality
because forages are not entirely substitutable. Dairy cows exhibit a small, but significant
response in milk yield when high quality forages are substituted for low quality forage in
otherwise equally balanced diets.
The values of three levels of quality within alfalfa and grass hay are calculated over the
period of January through March 2012. In alfalfa, nearly 65% of the total value is
associated with the NEL content, whereas in grass NEL content accounts for nearly 75% of
forage values. Of the 11 compositional inputs required in the calculation of hay and silage
values, NDF, lignin and ash appear to have the greatest importance.
INTRODUCTION
What Are Feeds Used For?
Animals do not require feeds; animals require nutrients. Feeds are nothing else than containers,
packages of nutrients. The sole value of a feed is in the value of the nutrients that it contains. A
feed containing no nutrient has no economic value. No economic value means that it is
worthless - ZERO.
What are the Nutrients of Economic Value?
The answer to that question depends on two things. First, the nutrients of economic value are
dependent on the class of animals under consideration. For example, the nutrients of economic
importance are not the same for beef cattle, lactating dairy cows, dry cows, and replacement
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animals. Hence a given feed has a different economic value to lactating dairy cows and
replacement heifers.
Second, the nutrients of economic value depend whether one is interested in the strategic value
of a feed versus its tactical value. This begs further explanations. A dairy producer feeding 50
lbs/day of a finely chopped corn silage is looking for attributes in purchased hay that are very
specific to the narrow conditions in which it is to be fed. The value of a given lot of hay to this
producer would be entirely tactical – i.e., determined by how well it fits as a complement to
other feed ingredients that are essentially pre-determined. On the other hand, a dairy producer
who considers all feed components of his dairy rations to be exchangeable (tradable) would look
at a given lot of hay with a strategic view. The hay would no longer be looked at as a
complement to other pre-determined feeds, but as a component of the whole diet. To put it
differently, tactical is when you have painted yourself in a corner; strategic is when you look at
the floor configuration before you start painting.
The economic values calculated in this paper are (1) exclusively for lactating dairy cows, and
(2) entirely strategic.
Of the large set of nutrients required by dairy cows, some have large economic values while
others have small economic values. The calcium content of feeds is a good example of a
nutrient with a small economic value. Calcium can be supplemented very inexpensively in any
dairy diets. This is not to say that calcium is not important to dairy cows or that ration balancing
should ignore calcium. It just says that the economics of feeding cows have little to do with
calcium.
We have extensively studied the major dairy feed markets in the U.S. over a period of 30 years.
Across all 3 major markets (Midwest, Northeast, West), two sets of nutrients explain over 98%
of the variation in feed prices. These are:
1. Net energy for lactation (NEL), rumen degradable protein (RDP), digestible rumen
undegradable protein (dRUP), effective neutral detergent fiber (eNDF), and non-effective
neutral detergent fiber (neNDF), or
2. NEL, metabolizable protein (MP), eNDF, and neNDF.
The two sets are entirely interchangeable and give very similar results. The protein
requirements of dairy cows, however, are best expressed as metabolizable protein. Therefore,
nutrient set #2 will be exclusively used in the balance of this paper.
UNIT PRICES OF IMPORTANT NUTRIENTS
Calculating Nutrient Unit Prices
Feed markets do exist: there are people selling and buying feeds in all major dairy regions. But
there is no market for nutrients. Or is there? Can we calculate the implicit nutrient prices from
the market prices of feedstuffs?
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The problem of determining the implicit price of attributes (the nutrients) embedded in various
products (feedstuffs) is no at all unique to the feed/nutrient complex. Economists have found an
elegant way to solve this problem using a method called hedonic pricing. We will not review
the details of how this work in this paper. Interested reader can consult St-Pierre and Cobanov
(2000) for further details. In short, prices and nutritional composition of all ingredients traded
in a given market are used to back-calculate, using statistical methods, what the markets are
implicitly pricing the nutrients contained in feeds. Market prices of nutrients in the Midwest for
the 86 months between January 2005 and March 2012 are shown in Figure 1. Southwest prices
would be a bit different, but the curves would largely parallel those for the Midwest.
Figure 1. Price of nutrients in the Midwest from January 2005 through March 2012. NEl$ =
Net energy for lactation ($/Mcal), MP$ = metabolizable protein ($/lb), and e-NDF$ = effective
NDF ($/lb).
During this period, the cost per unit of NEL has more than tripled, the cost per unit of MP has
doubled, while the cost per unit of eNDF has surged in the first half of 2011. The U.S. has
experienced drastic changes in renewable energy policies during the last decade, some of which
have had a substantial effect on feed prices. However, large variation in nutrient unit prices are
still evident even over a much shorter period of time such as what has occurred since January
2011 (Table 1).
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Table 1. Nutrient unit prices in the Southwest between January 2011 and March 2012.
Nutrients Average S.D. Min Max
NEL (¢/Mcal) 16.5 2.7 11.1 20.8
MP (¢/lb) 23.6 9.6 9.7 40.6
eNDF (¢/lb) 3.6 3.5 0.0 11.9
neNDF (¢/lb) -8.7 3.7 -13.5 -3.2
What Affects Nutrient Unit Prices?
Market prices of all feeds, not just the prices of corn, soybean meal and alfalfa hay, affect
nutrient unit prices. Therefore, nutrient unit prices change through time and location. We have
already shown how nutrients can quickly change through time in Table 1. Because of regional
differences in feed prices and availability, nutrient unit prices also show regional differences
(Table 2). In this paper we will be using southwest nutrient unit prices whenever this
information was available. When examining the effect of time, we will use January 2011 to
March 2012 prices.
Table 2. Nutrient unit prices across 3 regions1, December 2012.
Nutrients Midwest Southwest West
NEL (¢/Mcal) 15.8 13.7 15.9
MP (¢/lb) 38.9 49.7 35.3
eNDF (¢/lb) 4.0 5.6 6.9
neNDF (¢/lb) -3.2 -1.5 0.0
1 Midwest prices are for WI and eastern MN; Southwest prices are for northwest Texas; West prices are for
the San Joaquin Valley of CA.
Where Do I Find the Nutrient Unit Prices?
You can purchase a Windows-based software that we wrote (Sesame) for $10 at
www.sesamesoft.com. Beware that it is NOT the easiest software to use. Alternatively, we
publish a regular column in Progressive Dairyman where we publish the nutrient unit prices for
the major dairy regions of the U.S. Some nutrition consultants also provide this information to
their clients.
FORAGE COMPOSITION
Nutrient Composition Used in This Paper.
Each lot of forage has a unique nutrient composition that affects its value. The nutrient
composition of forages used as examples in this paper is reported in Table 3. We used 3 levels
of quality for legume hay and grass hay.
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Table 3. Nutrient composition of the reference alfalfa hay, reference grass hay, and low and
high quality hays used as examples.
Alfalfa Grass
Nutrients1 Units Reference Low High Reference Low High
Dry matter % 88 88 88 88 88 88
Crude protein % 20 16 24 12 8 16
NDICP % 2.5 2.5 2.5 4.0 4.0 4.0
ADICP % 1.5 1.5 1.5 1.0 1.0 1.0
Ether extracts % 2.0 2.0 2.0 2.5 2.5 2.5
NDF % 40 44 36 60 68 52
ADF % 30 34 26 40 48 32
Lignin % 7.0 8.8 5.4 6.5 8.5 4.5
Ash % 10 10 10 7 7 7
RUP %CP 25 25 25 30 30 30
RUPd % RUP 70 70 70 65 65 65
Effective NDF % NDF 92 92 92 98 98 98
TDN from
NFC
% 29.9 29.9 29.9 22.1 18.1 26.0
TDN from
NDF
% 15.4 15.8 14.8 28.3 30.8 25.9
TDN from CP % 18.3 14.3 22.3 10.9 6.9 14.8
TDN from EE % 2.3 2.3 2.3 3.4 3.4 3.4
TDN at 3X % 54.0 50.7 57.1 52.9 47.9 57.9
NEL at 3X Mcal/cwt 57.6 51.5 63.5 53.0 44.6 61.5
MP at 3X % 7.99 7.02 8.95 6.73 5.55 7.94
------------------------------ Units per Ton -----------------------------
NEL Mcal 1014.2 906.7 1118.1 932.6 785.5 1082.3
MP lbs 140.7 123.5 157.6 118.6 97.6 139.7
eNDF lbs 647.7 712.4 582.9 1034.9 1172.9 896.9
neNDF lbs 56.3 62.0 50.7 21.1 23.9 18.3
1 NDICP = NDF insoluble crude protein; ADICP = ADF insoluble crude protein; NDF = neutral detergent
fiber; ADF = acid detergent fiber; RUP = rumen undegradable protein; RUPd = RUP digestibility; TDN =
total digestible nutrients; NEL at 3X = net energy for lactation calculated at an intake of 3 times
maintenance; MP at 3X = metabolizable protein calculated at 3 times maintenance.
A few things are worth mentioning here. First, notice that the quality of alfalfa (and grass) has a
much smaller effect on its metabolizable protein than on its crude protein. Second, observe that
in alfalfa the non-fiber carbohydrates (NFC) contribute 2 times more to its energy content (i.e.,
TDN) than the NDF. In grass, the situation is reversed, with NDF contributing significantly
more to the energy content than NFC. Total tract NDF digestibility is greater in grass (~47%)
than in alfalfa (~39%) of equivalent quality.
How are NEL and MP Calculated?
Equations used in the calculation of NEL and MP according to NRC (2001) are reported in the
appendix. Although these equations may seem intimidating at first, they can easily be
programmed in a computer spreadsheet. While 9 chemical entries are required for the
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calculation of NEL only 5 measurements will have much effect on NEL in practice: DM, CP,
NDF, lignin, and ash. Other entries can simply be taken from standard feed composition tables.
The calculation of MP requires a measurement of CP, rumen degradability of protein
(RUP_CP), and post-ruminal digestibility of RUP (RUPd). Some feed laboratories provide
estimates of RUP_CP, but the variation within a type of hay is relatively small and largely
inconsequential to the value of the forage. Likewise, table values for RUPd should be used.
What NDF Digestibility Should be Used?
The ratio of lignin to protein-free NDF is used to estimate in vivo total tract NDF digestibility
(TT-NDFd) in the equation for TDN_NDF reported in the Appendix. The 2/3 exponent is used
to convert mass to surface area, hence representing the decrease in NDF digestibility due to the
surface interaction (i.e., coating) of cell walls by lignin. This conceptual interaction is
necessarily a simplification of the complex anatomy and chemistry of plant cell walls. Some
have advocated the use of in vitro NDF digestibility (NDFd) as a proxy for the calculated TT-
NDFd used when calculating TDN_NDF. Although this approach is appealing, much doubt
remains regarding the relationship between NDFd and TT-NDFd. For example, we have
summarized the relationship between TT-NDFd and NDFd for 23 diets where TT-NDFd was
measured using total fecal collection in trials conducted at our experimental research station
(Figure 2).
Figure 2. Relationship between whole diet total tract in vivo NDF digestibility (TT-NDFd)
expressed as deviation from a control diet and in vitro NDF digestibility (NDFd).
In this figure, it is apparent that NDFd overestimates differences between treatments and that the
magnitude of the difference in NDFd is not related to the magnitude of the difference in TT-
NDFd. The ranking within experiment was often OK with NDFd, raising the possibility of
using NDFd for energy calculation. It is clear, however, that NDFd cannot be directly
substituted for TT-NDFd when calculating the energy of a feed. Much work is needed in this
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area. Meanwhile, we still recommend using the equation with the ratio of lignin to protein-free
NDF for estimating the energy contribution of NDF.
CALCULATING THE VALUE OF A FORAGE
The Value of the Nutrients
So far, we have shown that nutrient unit prices can be calculated from market information from
all feedstuffs traded in an area. We also explained how the nutrient composition of forages for
the economically important nutrients is calculated. Determining the value of the nutrients in a
given forage involves a series of simple arithmetical operations. These are illustrated for the
reference alfalfa in Table 4 using the average price of nutrients for the Southwest from January
2011 to March 2012.
Table 4. Calculation of the value of the nutrients in one ton of the reference alfalfa hay using
average nutrient unit prices from January 2011 through March 2012.
Composition
DM
%
Mcal or
Pounds per
Ton
Unit Prices
¢
Value
$/ton
NEL (Mcal/cwt) 57.6 88 1014.2 16.5 167.34
MP (% DM) 7.99 88 140.7 23.6 33.20
eNDF (% DM) 36.8 88 647.7 3.6 23.31
neNDF (% DM) 3.2 88 56.3 -8.7 -4.90
Total 218.95
Correcting for Milk Production Response
For most feeds, the sum of the values of the nutrients as calculated in the preceding paragraph is
its average economic value; but not for forages. While most feeds are substitutable based on
their nutrient content, this is not entirely true for forages. What this means is that two rations
balanced for exactly the same nutrient density (NEL, MP, eNDF, neNDF) but using forages of
different quality do not result in exactly the same milk production. Cows fed the ration based on
a high quality forage respond to forage quality with additional milk production mainly through
greater dry matter intake (DMI). Note that this is not the same as the response to feeding
forages of different quality, but without any ration re-balancing. Here the rations are identical in
their nutritional content, but cows fed rations based on higher quality forages achieve a greater
level of milk production.
We used results from many research trials to calculate the response to forage quality. Although
one could think of a better marker of quality than the total NDF content of forage, the data did
not allow the calculation of anything more than NDF. The resulting equations used to calculate
the value per ton of forage due to milk production responses are:
Alfalfa: Value of Response ($/ton) = [(P-Milk x 0.273 x (44 – NDF)] x DM 100
Grass: Value of Response ($/ton) = [(P-Milk x 0.3 x (53 – NDF)] x DM 100
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where P-Milk is the price of milk ($/cwt). It is important to understand that this adjustment to
the value of forages means that forage values are dependent on milk prices. The difference in
the value of a high quality forage compared to that of a low quality forage is much smaller when
milk prices are low (such as in 2009) then when milk prices are high (as in 2011).
Effect of Forage Type and Quality on the Historical Value of Forages
Table 5 summarizes the values of alfalfa and grass hay for 3 levels of quality for the period of
January 2011 to March 2012. On an average, the range in values due to quality is greater in
grass ($124/ton) compared to alfalfa ($73/ton). This could be due to the arbitrary range of
quality selected for the two types of forages. On an average, alfalfa is worth $50/ton more than
grass. Compared to alfalfa, grass hay shows a greater range in value through time: $109 and
$126/ton for alfalfa and grass, respectively. More importantly, the value of forages changes
considerably through time even over a short time span.
Table 5. Value ($/ton) of alfalfa and grass hay of 3 quality levels, Southwest, January 2011 to
March 2012.
Feeds Average SD1
Min Max
Alfalfa - Reference 241 37 193 302
- Low 204 36 162 265
- High 277 38 223 338
Grass - Reference 191 46 145 271
- Low 129 47 77 210
- High 253 47 197 332
1 SD = standard deviation.
Contribution to Calculated Values
The value of a forage is the sum of the values of its important nutrients plus the milk response
associated with the forage quality expressed as NDF content. The contribution of each nutrient
to the value of a forage is not the same. Table 6 shows the average contribution of NEL, MP,
eNDF, neNDF, and milk response for the 15 months from January 2011 to March 2012 for the
reference alfalfa and grass hays. On an average, energy (NEL) content accounts for nearly 65%
of the value of alfalfa hay and 75% of the value of grass hay. Notice that the protein in alfalfa
(20% crude protein) is only worth $7/ton more than the protein in grass (12% crude protein).
This is because most of the protein in forage is rumen degradable (RDP), and the unit value of
RDP ($/lb) is generally null and often even slightly negative (results not shown). Producing
forages of greater protein content is of little value unless the protein increase is associated with
an increase in the digestibility (energy) of the resulting feeds.
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Table 6. Average contribution of NEL, MP, eNDF, neNDF, and milk response to the value of
our reference alfalfa and grass hays between January 2011 and March 2012.
Alfalfa Grass
Component $/ton % of Total $/ton % of Total
NEL 154.55 64.0 141.75 73.7
MP 43.75 18.2 36.88 19.2
eNDF 30.44 12.6 48.64 25.3
neNDF -4.78 -2.0 -1.79 -0.9
Milk 17.29 7.2 -33.26 -17.3
Total 240.86 100.0 192.21 100.0
In hay and most haycrop silages, most of the NDF is effective, resulting in very small neNDF
content (Table 2). Therefore, the contribution of neNDF to the value of long hays could be
entirely ignored without meaningful losses in the accuracy of estimating their economic values.
Marginal Changes from Compositional Values
The 4 nutrients used to calculate the value of a forage are calculated from 11 compositional
entries. We can calculate the change in the value of our reference alfalfa and grass hay from a
one-unit change in each of the 11 entries (Table 7).
Table 7. Marginal change in value of forage hay ($/ton) from a one-unit increase in each of the
compositional entries between January 2011 and March 2012.
Change in forage value ($/ton)
Composition entries Alfalfa - Reference Grass - Reference
Dry matter (%) 2.73 2.19
Crude protein (% DM) 2.12 2.23
NDICP (% DM) 1.28 1.14
ADICP (% DM) -5.17 -5.01
Ether Extracts (% DM) 4.72 4.72
NDF (% DM) -4.96 -5.10
Lignin (% DM) -4.42 -5.38
Ash (% DM) -3.68 -3.67
RUP (% CP) 0.76 0.43
RUPd (% RUP) 0.27 0.20
NDF Effectiveness (% NDF) 0.93 1.40
One should be extremely careful in the interpretation of these results. First, a one-unit change
does not represent the same degree of “difficulty” across all compositional elements. For
example, it is considerably easier to raise the NDF of grass by one unit than to raise its ether
extracts also by one unit. Second, and even more importantly, it is very difficult in nature to
change a compositional element by one unit without affecting any of the other compositional
elements. For example, crude protein in alfalfa is negatively associated with NDF content. On
average, raising crude protein lowers the NDF content (i.e., the plant is more immature).
Likewise, NDF and lignin content are positively associated, meaning that an increase in NDF
content is generally associated with an increase in lignin content.
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Keeping these reservations in mind, compositional elements can be loosely grouped into 3
categories.
1. Those with a small effect on the value of hay: RUP, RUPd and NDFe,
2. Those with a medium effect on the value of hay: DM, CP, NDICP, and
3. Those with a large effect on the value of hay: ADICP, ether extracts, NDF, lignin and ash.
Ether extracts and ADICP are relatively constant within hay type compared to NDF, lignin and
ash. NRC (2001) reports standard deviations of 0.4 (ADICP), 0.5 (ether extracts), 0.9 (lignin),
1.0 (ash), and 6.3 (NDF) percent. Thus, NDF, lignin, and ash are arguably the most influential
compositional entries to hay values. Note that the net effect of NDF on hay values incorporates
its positive effect on forage value from its positive contribution to eNDF, and its negative effects
on forage value from its negative contribution to NEL and MP.
CONCLUDING REMARKS
The values calculated in this paper are on a farm-gate basis (i.e., delivered) and not FOB.
Therefore, forage growers would have to account for delivery costs when estimating the value
of a given hay or silage. In addition, the values calculated in this paper are averages and
represent what coherent buyers should be willing to pay. Coherent behavior is often an elusive
attribute in feed markets. Some buyers consistently shop for “supreme” quality alfalfa hay
because that’s what they have been using for years without ever considering whether other
quality levels or even other types of feeds make more economic sense. A very thirsty man is
much more willing to pay an exorbitant price for a cold beer, especially if he fails to consider
the free water available from a nearby fountain.
REFERENCES
St-Pierre, N. R., and D. Glamocic. 2000. Estimating unit costs of nutrients from market prices
of feedstuffs. J. Dairy Sci. 83:1402-1411.
APPENDIX
Equations used to calculate NEL (NE_3X, Mcal/lb) of forages:
TDN_NFC = 0.98 x (100 – NDF + NDICP – CP – EE – ASH)
TDN_NDF = 0.75 x (NDF – NDICP – LIG) x (1-(LIG/(NDF-NDICP))0.667
)
TDN_CP = CP x exp(-1.2 x ADICP/CP)
TDN_EE = (EE – 1) x 2.25
TDN_1X = TDN_NFC + TDN_NDF + TDN_CP + TDN_EE - 7
DE_1X = (TDN_NFC x 0.042) + (TDN_NDF x 0.042) + (TDN_CP x 0.056)
+ ((EE-1) x 0.094) - 0.3
TDN_3X = TDN_1X x 0.92
NE_3X = (0.6532 x DE_1X) - 0.5064
Equations used to calculate the metabolizable protein (MP, % of DM) of forages:
dRUP = CP x RUP_CP x RUPd 10000
dMTP = TDN_3X x 1.3 x 0.64 10
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MP = dRUP + dMTP
Equations used to calculate effective and non-effective NDF of forages:
eNDF = NDF x NDFe
neNDF = NDF - eNDF
where:
ADICP = ADF insoluble crude protein (% of DM)
ASH = Ash (% of DM)
CP = Crude protein (% of DM)
dRUP = Digestible RUP (% of DM)
dMTP = Digestible microbial true protein (% of DM)
EE = Ether extracts (% of DM)
eNDF = Effective NDF (% of DM)
exp = The exponential function (i.e., e exponent the value in parentheses)
LIG = Lignin (% of DM)
NDF = Neutral detergent fiber (% of DM)
NDFe = NDF effectiveness (% of NDF)
NDICP = NDF insoluble crude protein (% of DM)
NE_3X = Net energy for lactation measured a 3 times maintenance (Mcal/lb)
neNDF = Non-effective NDF (% of DM)
RUP_CP = Rumen undegradable protein (% of CP)
RUPd = Digestibility of RUP (% of RUP)
TDN_1X = Total digestible nutrients at 1 time maintenance (% of DM)
TDN_3X = Total digestible nutrients at 3 times maintenance (% of DM)
TDN_CP = TDN from the crude protein fraction (% of DM)
TDN_EE = TDN from the ether extracts fraction (% of DM)
TDN_NDF = TDN from the NDF fraction (% of DM)
TDN_NFC = TDN from the NFC fraction (% of DM).
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Managing Heat Stress and its Impact on Cow Behavior
J.D. Allen
1, S.D. Anderson
2, R.J. Collier
2, and J.F. Smith
2
1Northwest Missouri State University, [email protected]
2University of Arizona, Tucson, AZ, [email protected], [email protected],
SUMMARY
Heat stress affects several aspects of the dairy industry including cattle behavior.
Heat stress will increase an animal’s standing time as it tries to dissipate heat over its entire
body surface.
Increasing standing time or decreasing resting time reduces milk production.
Prolonged standing further increases the risk of lameness.
Understanding environmental and physiological parameters that affect standing behavior
will improve industry efforts to minimize heat stress in dairy cattle.
Core body temperature is correlated standing behavior, with cattle more likely to stand
above a 102.07 °F (39.2 °C) core body temperature.
Correlation between thermal heat index and cattle behavior has also been evaluated,
although predictive capacity has yet to be established. However, cattle are more likely to
stand above a THI of 68.
INTRODUCTION
The issue of environmental impacts on dairy production and cattle welfare has long been of
interest to the industry. One environmental stressor which has commanded considerable
research attention within the past several decades has been thermal stress. Production loss due to
heat stress has been estimated at $900 million annually to U.S. dairy herd (St. Pierre et al.,
2003). This interest in heat stress has coincided with the spreading demographic of the United
States dairy industry from the Midwest to warmer and more arid climates, such as the desert
Southwest as well as an increase to heat sensitivity due to a doubling of average production per
cow. Improvements in warm weather dairy housing have provided more efficient technologies
for cooling animals exposed to hot climates. However, heat stress remains an important
environmental stressor on dairy cattle.
Heat stress directly and indirectly affects feed intake, cow body temperature, maintenance
requirements and metabolic processes, feed efficiency, milk yield, reproductive efficiency, cow
behavior, and disease incidence (Thatcher, 1974; Cook et al., 2007; Tucker et al., 2007; Rhoads
et al., 2009). These effects are well documented. It is only recently that researchers have
attempted to understand the correlation of one of the most understood outcomes (increased body
temperature) to one of the least understood outcomes (modified cow behavior) and its possible
effect on bottom line production.
HEAT STRESS AND DAIRY CATTLE
Domestic animals have a core body temperature (CBT) range in which metabolism functions
without modification, termed the thermoneutral zone. Typically, core body temperature is higher
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than ambient temperature to ensure that heat generated by metabolism flows out to the
environment (Collier et al., 2006). Deviation outside of this range – which is relatively narrow –
leads to increases in resting metabolism, modifications to the biochemistry and cellular
physiology as well as the behavior of the animal (Shearer and Beede, 1990). The thermoneutral
zone lies between 41 and 77 °F (5 and 25 °C) for dairy cattle (Roenfeldt, 1998). Above 77 °F
(25 °C), the body must modify physiology and behavior to keep CBT above the environment
temperature.
HEAT STRESS AND THERMAL HUMIDITY INDEX
Temperature is not the only environmental factor that affects the intensity of heat stress. The
temperature humidity index (THI) measures the combined effects of ambient temperature and
relative humidity (RH) to ascertain heat load intensity (Berry et al., 1964). This index was later
categorized into heat stress levels with an index above 72 THI [75 °F (23.9 °C) with 65% RH to
90 °F (32.2 °C) with 0% RH] established as the lower threshold of heat stress (Whittier, 1993;
Armstrong, 1994). However, because of the increase of milk production per cow since the
development of the THI, a 22 lbs/d (10 kg/d) increase will decrease the threshold for heat stress
by 9 °F (5 °C; Berman, 2005). A recent re-evaluation of the THI has suggested that due to this
improvement of milk production, the THI heat stress threshold should be lowered to 68 [72 °F
(22.2 °C) with 45% RH to 80 °F (26.7 °C) with 0% RH; Zimbelman et al., 2009].
HEAT STRESS AND REPRODUCTION
Elevated core body temperature (CBT) in dairy cows caused by heat stress can have detrimental
effects on reproductive performance. An increase in rectal temperature of 1.8 °F (1 °C)
occurring 12 h post-insemination decreased pregnancy rates by 16% (Ulberg and Burfening,
1967). Gwazdauskas et al. (1973) reported an increase in uterine temperature of 0.9 °F (0.5 °C)
on the day of or the day after insemination resulted in decreased conception rates by 13% and
7%, respectively. Badinga et al. (1985) attributed decreased conception rates of lactating cows
to their inability to maintain normal body temperature at high environmental temperatures
[> 86 °F (30 °C)]. Ealy and colleagues (1993) further support this hypothesis by reporting that
bovine embryos become more resistant to adverse effects of maternal heat stress as pregnancy
progresses. Embryos are sensitive to deleterious effects on d 1 following artificial insemination
but develop substantial resistance by d 3. Expression of estrous behavior is also depressed when
cows become heat-stressed.
Prolonged heat stress negatively affected reproduction by increasing estrous cycle length and
decreasing duration of estrus (Abilay et al., 1975). A decrease in the frequency of pulsatile
release of luteinizing hormone on d 5 of the estrous cycle was observed in heat-stressed cows
compared to cooled cows (Wise et al., 1988). Follicular dynamics are altered and follicular
dominance is depressed by heat stress (Wolfenson et al., 1995). Furthermore, fetal growth is
negatively affected due to decreased uterine blood supply and the insufficiency of the placenta
to provide maternal nutrients (Collier et al., 1982).
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HEAT STRESS AND MILK PRODUCTION
When cows are subjected to heat stress, feed intake decreases. Simultaneously, maintenance
requirements are increased due to activation of the thermoregulatory system. There is need to
expend energy to maintain homeothermy that would otherwise be available for useful
production (e.g. milk; Buffington et al., 1983). Mild to severe heat stress in dairy cattle has been
estimated to cause an increase in maintenance requirements by 7 to 25% (NRC, 2001). By
definition, heat-stressed cows are in a state of negative energy balance (NEBAL) since feed
intake is not meeting energetic demands of maintenance and lactation.
Decreased intake accounts for approximately 36% of the decrease in milk production due to
shifts in postabsorptive metabolism and nutrient partitioning (Rhoads et al., 2009). Under
thermoneutral conditions, cows experiencing NEBAL have increased rates of lipolysis. This is
characterized by the presence of elevated plasma nonesterified fatty acid (NEFA)
concentrations, while glucose is partitioned to the mammary gland for milk synthesis. However,
heat-stressed cows have lower NEFA concentrations and a higher rate of peripheral glucose
utilization, suggesting that glucose uptake by other tissues reduces the amount of glucose
available for milk synthesis (Rhoads et al., 2009).
A reduction in feed intake precedes a decrease in milk production when cows are subjected to
heat stress (Rhoads et al., 2009). Spiers et al. (2004) showed that feed intake decreased within 1
d after initiation of heat stress, while milk yield decreased after d 2 of heat stress. Collier et al.
(1981) demonstrated that maximum decrease in milk yield during heat stress occurs 48 hours
after the initiation of the stress.
Prolonged thermal stress negatively impacts somatotropin (growth hormone or GH) secretion
from the anterior pituitary (Mitra et al., 1972). Depressed GH concentrations result in slower
growth rates, reduced nitrogen retention, and contribute to decreased lactation performance in
dairy cattle (Mitra et al., 1972).
Johnson et al. (1963) reported that milk yield decreased by 4 lbs/d (1.8 kg/d) per cow for every 1
°F (0.55 °C) increase above a daily rectal temperature of 101.5 °F (38.6 °C). More recently,
Igono et al. (1985) reported that a cow with a mean rectal temperature of 102.4 (39.1 °C)
produced 1.54 lbs/d (0.7 kg/d) less milk than a cow with a rectal temperature of 101.8 °F (38.8
°C). Zimbelman et al. (2009) also reported a negative relationship between rectal temperature
and milk production. This is relationship is further complicated with higher internal heat
production in high producing cows compared to low producing cows, regardless of
environmental influence (Purwanto et al., 1990).
HEAT STRESS AND PRODUCTION EFFICIENCY
There are a number of behavioural, physiological and metabolic mechanisms which are
employed by the cow to keep CBT above environmental temperature. Some of these are shown
in Figure 1.
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71
Figure 1. Schematic of the general effects of heat stress in dairy cows. (Adapted from Atrian
and Shahryar, 2012).
Energy production and expenditure through cellular maintenance produces excess metabolic
heat. Thus, heat exchange from the animal to environment is necessary to maintain optimal CBT
(Kadzere et al., 2002). A negative correlation between metabolic hormones (thyroid hormones,
somatotropin, prolactin, etc.) has been reported (Mitra et al., 1972; Johnson et al., 1988; Lu
1989; Collier et al., 2006). These hormones are responsible for energy expenditure and heat
production, including gut motility and blood flow to the digestive system (Hales et al., 1984;
Johnson et al., 1988). A decrease in gut motility leads to slower passage rate, decreasing feed
intake. West (2003) reported a 1.9 lbs (0.85 kg) decrease in dry matter intake with every 1.8 °F
(1 °C) increase in ambient temperature above a cow’s thermal neutral zone. While digestion is
improved, the lowered amount of feed within the digestive system is unable to meet
requirements (Kadzere et al., 2002), decreasing feed efficiency.
Physiological mechanisms which improve heat dissipation also lead to an increase in
maintenance requirements because of an increase in nutrient needs. Examples include increased
respiration rate, increased sweating, increased heart rate, and increased salivation (Atrian and
Shahryar, 2012). These in turn lead to increased body fluid loss which further increases
maintenance requirements to abate dehydration and blood homeostasis (Collier et al., 2006).
While these actions may seem futile, 15% of total body heat loss can be realized through normal
respiration (McDowell et al., 1976), and increased respiration rate can and does increase heat
loss potential (Campos Maia, et al., 2005).
Together, the cow’s adaptation to minimizing heat production and maximizing heat dissipation
leads to economic issues. Milk production will decrease, but energy and nutrient usage by the
cow will increase. With an increase in maintenance requirements compounded by a decrease in
dietary nutrients, nutrients are diverted from systems not necessary for survival. Rhoads and
others (2009) reported a significant repartitioning between dietary and body nutrients utilized
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for milk production during heat stress, with decreased feed intake accounting for only 36% of
milk production loss. Smith and others (2008) calculated that at a milk price of $18/cwt
($39.50/100 kg), a 2 to 12 lbs (0.9 to 5.5 kg) drop in milk production per cow per day due to
heat stress could cost an operation between $32 [2 lbs/d (0.9kg/d) loss for 90 days] and $324 [12
lbs/d (5.5 kg/d) loss for 150 days].
HEAT STRESS AND HEALTH
Other than the physiological issues that arise from heat stress adaptation, there is ample research
linking heat stress to particular aspects of an animal’s health. Specifically, lameness incidence
increases with an increase in ambient temperature (Cook et al., 2007). This coincides with the
change of seasons as well; lameness prevalence is lower in cool months as compared to warm
months (Sanders et al., 2009). These climatic and seasonal effects are also correlated to mastitis
(Dohoo and Meek, 1982; Elvinger et al., 1991). Several trials have reported an increase of
disease, particularly reproductive issues, during warmer months of the year due to the
acceptable environment for pathogens and vectors (Collins and Weiner, 1968; Silanikove, 2000;
Kadzere et al., 2002). Death losses also increase with an increase in THI (Vitali et al. 2009).
Recent interest has also hinted at the effect of cow behavior on increased risk for locomotive
diseases.
HEAT STRESS AND COW BEHAVIOR
Within the last decade, research efforts have turned to welfare of cattle experiencing heat stress.
With an increase in ambient temperature or solar radiation, cattle are more likely to seek shades
or other cooling structures (Tucker et al., 2008; Atrian and Shahryar, 2012). This change in
behavior, aside from the physiological changes to decrease heat production mentioned above,
suggests that dairy cows will also seek micro-environments that have a lower ambient
temperature. Furthermore, cattle are more likely to seek optimum environments that have
maximized cooling capacity. For instance, a recent study reported cattle were more likely to
choose shade over a cooling system directed away from the shade, but were also likely to take
advantage of shade that included a cooling system (Anderson et al., 2012).
To maximize heat loss regardless of environment, dairy cattle in areas with elevated temperature
often stand to increase available surface for heat dissipation (Igono et al., 1987; Anderson et al.,
2012, Smith et al., 2012). Even a mild increase in ambient temperature can invoke an increase in
standing time (Smith et al. 2012). Highest incidence of lameness (new cases) occurs when cattle
stand longer than 45% of the day (Galindo and Broom, 2000), and locomotion scores increase
during summer months relative to winter months (Cook et al., 2007). A negative correlation
between time spent lying and incidence of lameness as well as time spent lying and temperature
humidity index has also been reported (Leonard et al., 1996; Privolo and Riva, 2009). This
suggests that cattle exposed to higher temperatures are more likely to stand to improve heat
dissipation but are also more likely to experience periods of lameness during the same time
frame. Reducing resting time has been reported to reduce milk production (Bach et al., 2008,
Grant 2007). It was estimated that for each hour of increased resting time that milk production
increased 3.7 lbs (1.7 kg).
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The effects of lameness on dairy production are compounded by and just as disconcerting as
heat stress effects. Lameness affects resting and feeding behavior (Cook et al., 2007), decreases
reproduction efficiency (Garbarino et al., 2004), and increases the likelihood for early removal
from the herd (Collick et al., 1989). In hot climates, cattle are forced to risk lameness or risk
overheating.
CBT AND COW BEHAVIOR
To further our understanding of behavioral conditions of heat stressed dairy cows, we combined
three different data sets from heat stress trials conducted in Arizona (Anderson et al., 2012),
California (S. Rungruang, unpublished), and Minnesota (Smith et al., 2012). In each trial,
lactating dairy cows were fitted with 2 data loggers: one recorded CBT intra-vaginally, and one
recorded angle of leg to determine lying status. All data were standardized to 5-minute intervals
for CBT or 15-minute intervals for ambient conditions, and 2 hours per each milking period
were removed to eliminate human interference and subsequent feeding.
While mild temperatures in the Minnesota trial resulted in higher lying CBT, the 2 other
climates revealed greater incidence of heat stress and higher standing CBT compared to lying
CBT (Figure 2). Table 1 shows the narrow CBT range (0.11 °F or 0.06 °C) of cattle standing
compared to cattle lying. Altogether, CBT during posture shift (lying to standing or standing to
lying) was equal (Table 2), suggesting that dairy cattle may be cognizent of their fluctuating
CBT and are reacting preemptively to battle a dramatic shift in CBT, regardless of time of day
(Figure 3).
Figure 2. Cumulative core body temperature relation to posture in lactating dairy cows.
Treatments are designated as follows: 1 = Arizona with fixed fans and misters under drylot
shade; 2 = Arizona with adjustable fans and misters under drylot shade; 3 = Minnesota within a
cross-ventilated building; 4 = Minnesota within a cross-ventilated building with evaporative
pads; 5 = California with feed-line soakers and fans; and 6 = California with hydrothermally
cooled freestalls without feed-line soaking or fans. A treatment effect is observed (P < 0.0001).
Columns within treatment with different letter designations differ (P < 0.01).
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Table 1. Core body temperature of lactating dairy cows in relation to posture1
Posture
Item: Standing Lying SEM P Value
Core Body Temperature, °F
(°C)
103.834
(39.908)
101.912
(38.840)
0.0025
(0.0014)
0.0001
1 Data is representative of cows in Arizona (n = 56), California (n = 37), and Minnesota (n =
64).
Table 2. Core body temperature of lactating dairy cows in relation to posture1
Posture
Item:
Initial
Stand
Continuance
of Stand
Initial
Lying
Continuance of
Lying
SEM
Core Body
Temperature, °F
(°C)
102.144a
(38.969)
101.916b
(38.842)
101.847c
(38.804)
101.917b
(38.843)
0.0085
0.0047
a,b,c Letters in the same row with a different superscript differ (P < 0.0001).
1 Initial lying is representative of the period in which the animal has transitioned from a
standing to lying posture; continuance of lying is representative of the period after the animal
has initially lied down. Data is representative of cows in Arizona (n = 56), California (n = 37),
and Minnesota (n = 64).
Figure 3. Effect of period of day on core body temperature of standing and lying bouts (Period
effect: P < 0.01)
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An analysis of the entire data set (> 260,000 data points) provided a correlation (r2 = 0.56, P <
0.0001) between CBT and cow posture, giving researchers and producers a more specific CBT
in which to focus their attention when managing dairy cattle for heat stress and cow comfort. In
this data set cattle were more likely to be standing at a CBT greater than 38.93 °C (102.07 °F;
Figure 4).
This does not suggest that cows with a CBT below this mark do not experience heat stress.
However, with increased standing behavior as an indicator of heat stress, this CBT provides a
point at which to improve our management efforts to alleviate the negative affects of heat stress,
particularly in decreasing the amount of time a cow stands to dissipate body heat.
Figure 4. Percent of animals standing in relation to core body temperature. Data is
representative of cows in Arizona (n = 56), California (n = 37), and Minnesota (n = 64).
Data using THI as a predictor of stance were limiting in predictive power (r2 < 0.20). This may
be in part to the diminished number of THI data points (< 90,000) as compared to the CBT data
points (> 260,000). However, the impact of THI on cattle behavior is measurable (Table 3) and
appears to follow the same pattern as CBT. Although not specified, the 50 percent mark would
occur just above a THI of 71, which is just above a THI of 68, the established threshold where
heat stress begins in high producing dairy cows (Zimbelman et al., 2009).
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Table 3. Percent of cattle standing within THI categories1
THI Category2
Item: < 68 68 to 71 72 to 79 80 to 89 90 to 98 > 100 SEM
Animals
Standing, %
43.6
49.8
53.0
68.2
49.7
52.2
1.6 1 P < 0.0001. Data is representative of cows in Arizona (n = 56), California (n = 37), and
Minnesota (n = 64). 2 Categories defined as thermal neutral (< 68), heat stress threshold (68 to 71), mild-moderate
heat stress (72 to 79, moderate-severe heat stress (80 to 89), severe heat stress (90 to 98), and
extremely severe heat stress (> 100).
SUMMARY
Heat stress is a major economic issue in the dairy industry. Its effects reach beyond milk
production into reproduction, health, and welfare arenas through physiological and behavioral
changes. Modifications to cow behavior are linked to overall production performance and
should not be over-looked. Improving the cow’s comfort by reducing the amount of time it
stands to dissipate heat can ultimately reduce the affect of heat stress on milk production.
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Whittier, J. C. 1993. Hot weather livestock stress. Univ. Missouri. Ext. Bull. G2099. Mt.
Vernon.
Wolfenson, D., W. W. Thatcher, L. Badinga, J. D. Savio, R. Meidan, B. J. Lew, R. Braw-Tal,
and A. Berman. 1995. Effect of heat stress on follicular development during the estrous
cycle in lactating dairy cattle. Biol. Repro.52:1106-1113.
Zimbelman, R. B., R. P. Rhoads, M. L. Rhoads, G. C. Duff, L. H. Baumguard, and R. J. Collier.
2009. A re-evaluation of the impact of temperature humidity indx (THI) and black
globe temperature humidity index (BGHI) on milk production in high producing dairy
cows. Proceedings of the 24th
Southwest Nutrition and Management conference,
Tempe, AZ. pp. 158-168.
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Early Weaning Beef Calves to Improve Herd Productivity: Implications on
Cow and Calf Nutrition
J. D. Arthington
Range Cattle Research and Education Center, Ona
University of Florida – IFAS
SUMMARY
Early calf weaning is not new to the science of beef cattle production. The benefits of early
weaning during instances of environmental strain, usually witnessed by a shortage of summer
forage, has been understood and practiced for many years. However, the use of early weaning
as a normal, annual management practice for first-calf cows is much less common. Our interest
in the topic originated from the common production practice in the Southeast, which allowed
heifers to develop for two years before being bred the first time. Calving heifers for the first
time at three years of age is quite common across production regions that utilize a high
percentage of Bos indicus lineage (i.e. Brahman). Compared to heifers of traditional English
lineage (Bos taurus), Brahman-crossbred heifers have been shown to have lower calving rates
when developed to calve at 24 months of age (DeRouen and Franke, 1989). The reason relates
to the slow rate of maturity common to Bos indicus cattle, witnessed by both delayed onset of
puberty (Rodrigues et al., 2002) and increased time required to achieve mature body size
(Martin et al., 1992). Nevertheless, heifers that calve for the first time at three years of age have
reduced lifetime economic efficiency than those managed to calve at two years of age.
Although, calving at three years of age may increase repeatability of pregnancy, forcing all two
year olds to remain non-productive an entire year decreases the overall economic efficiency of
the cowherd (Nunez-Dominguez et al., 1991).
INTRODUCTION
In beef production systems, early weaning lacks an appropriate definition. In most regions of
the US, beef calves are weaned from their dams at approximately six to eight months of age.
Therefore, any calves weaned prior to six months of age may be considered, “early weaned”.
For our purposes, early weaning refers to the permanent separation of the calf from its mother at
approximately 90 days of age. This target age is used to ensure that the process of early
weaning has an opportunity to impact the reproductive performance of the cow. Calves weaned
at four and five months of age may be mistakenly referred to as “early weaned”, but this is truly
a misnomer, as the cow will benefit little reproductively within a fixed breeding season. By this
age, the breeding season has likely ended or almost over once the calf is weaned. To harvest the
most efficiency from the effort, early weaning should always occur at the start, or very near the
start, of the normal breeding season. It has been our experience, and the experience of others
(Dr. Ron Lemenager, Purdue University; personal communication) that beef calves should not
be weaned when they are less than 50 days of age. When weaning at ages less than 50 days, we
have found that calves perform poorly and appear to be stunted, never recovering their normal
body weight even many months later. This age threshold is supported by the common age at
which dairy calves begin consuming significant amounts of dry feed. Dairy producers begin the
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transition process from liquid milk to complete dry feeds when calves reach 45 to 50 days of
age. Therefore, the target age for early weaning beef calves should be 50 to 90 days of age.
THE COW
Body Condition
Assuming the beef herd is otherwise healthy, nothing impacts cowherd reproductive
performance than prolonged post-partum anestrus – and nothing impacts post-partum anestrus
more than cow body condition. Low cow body condition is the primary reason for reduced
conception rates and overall poor cowherd productivity. Cow body condition is a subjective
estimate of the amount of fat on a cow and is the most reliable method for evaluating a
nutritional program. Body condition typically declines after calving, when the nutritional
demands of the cow are at a maximum. It is during this time that supplemental nutrition is most
needed. Research from the University of Florida (Rae et al., 1993) has shown that cows with
low body condition scores (≤ 4.0) have a 30% reduction in pregnancy rate compared to cows in
optimum body condition (5.0 to 6.0). The low body condition score cows that do conceive often
do so late in the breeding season. This increase in post-partum interval results in later calves the
following year. This is most pronounced in young cows, which possess higher nutritional
demands to support both lactation as well as their own continued growth. When managing these
young cows, producers are faced with a limited number of options, including, 1) provide
adequate nutrient-dense supplementation, 2) early weaning, therefore removing the nutritional
demands associated with lactation, or 3) breed heifers at 3 years of age when their own growth
demands are lessened. We examined the influence of early weaning on first-calf cow body
weight and body condition score change over two consecutive years (Arthington and
Kalmbacher, 2003). In our study, early weaning resulted in a 2-point increase in cow body
condition score compared to contemporary cows nursing their calves up to the time of normal
weaning. (Table 1). This difference in body condition score allows the cows to calve in the
following year with greater condition, which optimizes their chances to rebreed early resulting
in older, heavier calves at weaning the next year.
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Table 1. Effect of early- versus normal-weaning on first-calf heifer BW and
body condition (average of two consecutive years)
Treatment
Item EW NW SEM
Heifer BW, lb a
January 922 c 955
d 11.2
April 988 d 946
c 9.7
August 1,083 d 997
c 11.0
Change 161 d 42
c 7.1
Heifer BCS b
January 4.28 4.28 0.10
April 5.42 d 4.46
c 0.11
August 6.34 d 4.75
c 0.07
a Individual heifer BW collected at the time of early weaning (EW; January),
when calves came off ryegrass (April), and at the time of normal calf weaning
(NW; August) (n = 50 and 58 for EW and NW, respectively). b Heifer body condition score (BCS) recorded as an average of two
technicians at each collection date using a 1 to 9 scale (1 = emaciated and 9 =
obese). c,d
Treatment means within a row without a common superscript letter differ (P
< 0.05).
Feed Intake
Early weaning may be a practical and profitable management consideration for cow/calf
operations. As early-weaned cows begin to stop lactating, their dry matter intake decreases by
as much as 30%. Results from our research (Arthington and Minton, 2004) have shown that
early-weaned, first-calf cows require approximately 50% less TDN to achieve and maintain a
body condition score of 5.0 compared to lactating heifers of the same age and body condition
(Figure 1). The intake values represented by these data show the amount of TDN consumed by
a lactating first-calf cow, plus her calf, compared to an early-weaned first-calf cow without her
calf. These data suggest greater than a 40% improvement in converting TDN into calf gain.
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Figure 1. Effect of early calf weaning on voluntary dry matter intake of TDN
in first-calf cows. Early-weaned calves were removed on the first d of wk 1.
5
10
15
20
25
Initial 1 2 3 4 5 6 7 8 9 10
Early Weaned
Normal Weaned
Weeks following early weaning
TD
N in
take,
lb/d
This voluntary decrease in dry matter intake has important practical implications for the
cow/calf producer, whereas the cow can maintain or gain body weight with almost 30% less
forage. In one study (Galindo-Gonzalez et al., 2007), the effect of cow parity (primi- versus
multiparous) and early weaning on hay intake, cow body weight and condition change, and
pregnancy rate was investigated. In that study, there was very little difference in the effect of
parity when measuring cow response to early weaning. Our original hypothesis stated that
young, primiparous cows would realize a greater production response to early weaning versus
mature, multiparous cows when each were compared to normal-weaned contemporaries of a
similar parity. This was not the case, as mature cows also experienced a considerable decrease
in hay dry matter intake concurrent with an increase in body condition and pregnancy rate. In
this study, cows with their calves consumed approximately 18% more hay than early-weaned
cows. This value differs from the 30% decrease suggested earlier due to the presence of winter
perennial pasture. The hay was a supplement to pasture and pasture forage intake was not
measured. The response summary over two yeas (n = 96 cows) for both primi- and multiparous
cows is provided in Table 2. Considering a 100 day winter hay supplementation period and hay
valued at $100/ton, early weaning can save nearly $12 per cow in hay costs alone. This
production efficiency estimate does not take into account the value of increased pregnancy rate
and decreased post-partum interval, which are the primary benefits realized by early weaning.
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Table 2. Effect of early weaning on supplemental hay intake and performance of beef cows
wintered on perennial bahiagrass pasture (average of two years; n = 96 cows).
Item Early-weaned Normal-weaned SEM P =
Hay intake, lb/cow/d a 14.2 16.7 0.5 < 0.01
Body condition change a,b
+ 0.5 - 0.5 0.08 < 0.01
Pregnancy rate, % 80.4 69.6 ----- 0.23 a Calves early weaned at an average age of 85 days. Hay intake and body condition
change calculated for 75 days after early weaning, after which all cows were exposed
to mature bulls as a single group for 45 days. b Body condition scored on a 1 to 9 scale (1 = emaciated and 9 = obese).
Reproductive Performance
The removal of a calf from a post-partum, anestrous cow results in an endocrine response
initiating estrus. The common management system involving a 48-hour calf removal is targeted
at initiating this response by removing the suckling stimuli. Early calf weaning creates the same
scenario, but in this case the calf is not returned to the dam. In one study, we evaluated the post-
partum interval of thin, first-calf heifers which were early-weaned or allowed to remain with
their calf (Arthington and Minton, 2004). We fed each heifer individually to ensure similar
amounts of body weight gain over 70 days. By the end of the feeding period, cows from both
treatments gained a similar amount of body weight and body condition; however, more early-
weaned cows were cycling compared to normal-weaned contemporaries (Figure 2). These data
suggest that the calf-removal response is an important factor affecting post-partum anestrus,
independent of nutrition.
Figure 2. Effect of early calf weaning on post-partum cyclicity of first-calf heifers. Early-
weaned calves were removed on the first d of wk 1. Date of return to estrus was determined as
the first wk when progesterone concentrations were greater than 1 ng/mL for two consecutive
weekly samples.
0
10
20
30
40
50
60
70
80
90
100
Initial 1 2 3 4 5 6 7 8 9 10
Early Weaned
Normal Weaned
Weeks following early weaning
Co
ws c
yclin
g,
% *
* * *** ** ** ** ** **
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In some situations, producers may be unable or unwilling to permanently separate beef calves at
these early ages. Recently, we compared the reproductive effects of 5 consecutive 48-h calf
withdrawals (20 d apart) to permanent calf withdrawal (early weaning) and a traditional single
48-h calf withdrawal (Martins et al., 2012). In that study, first-calf cows that were early-weaned
or exposed to multiple calf withdrawals attained post-partum cyclicity at the same rate and
sooner than first-calf cows that were submitted to a single 48-h calf withdrawal (Figure 3).
Although, the multiple calf withdrawals mimicked permanent separation in terms of hastened
post-partum anestrus, cows with unweaned calves had lesser body weight gain and a greater
body condition decline compared to early-weaned cows throughout the breeding season.
Figure 3. Percentage of cows cycling during the 90-d breeding season. Early-weaned cows had
their calves permanently removed at the start fo the breeding season (day 0); controlcows had
their calves removed for 48 h once at the start of the breeding season; interval-weaned cows had
their calves removed for 48 h five times, 20 d apart throughout the breeding season. a,b; P <
0.05.
0
10
20
30
40
50
60
70
80
90
100
0 10 20 30 40 50 60 70 80 90
Early-weaned
Interval-weaned
Control
Day
Perc
ent
cycling
a
ab
b
a
ab
b
a
a
a
a
a
a
b
b
b
b b
a
aa
a
In any given year, the majority of cows in a producer’s non-pregnant category are heifers and
young cows. The use of early weaning will allow these females to regain their lost body
condition, and do so with less forage and supplemental feed. As well, the decrease in post-
partum interval means these females will become pregnant earlier in the breeding season and
produce calves that will be older and heavier at next year’s weaning. In a two-year study,
investigating two-year old first calf heifers, we reported a greater pregnancy rate and a 21-day
shorter calving interval in early-weaned versus normal-weaned cows of a similar age (89.5
versus 50.0 % pregnant for early- and normal-weaned cows, respectively; Arthington and
Kalmbacher, 2003). The greatest economic advantage of early calf weaning is realized through
increased pregnancy rate of otherwise anestrous cows. Although our data suggests that early
weaning also improves the performance of mature cows, the major advantage to the system is
allowing heifers to be bred as yearlings, calve at two-years of age without suffering losses in
body weight and poor subsequent fertility as a lactating two-year old.
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THE EARLY-WEANED CALF
Nutritional Management
Depending on the region of production, producers may or may not have forage resources to
graze early-weaned calves. Some of the research studying the effects of early weaning on calf
productivity in the mid-west and high-plains regions of the US have focused on drylot feeding
of the early-weaned calves. In warmer climates, producers may be able to graze calves on
perennial or annual pastures throughout the year. In our experiences, opportunities to rear early-
weaned calves on high-quality pasture forage provide an important value toward the costs of
maintaining an early-weaned calf.
Early-weaned calves respond favorably to supplemental concentrate, even when they have are
grazing highly nutritious pastures, such as annual winter ryegrass (Figure 4). In a study
investigating the performance of early-weaned calves grazing winter ryegrass pastures
(Vendramini et al., 2006), voluntary forage intake decreased and calf ADG increased as the rate
of supplementation increased from 1.0, 1.5, and 2.0% of body weight (Table 3).
Table 3. Performance of early-weaned calves grazing winter rye-ryegrass pastures
and supplemented with different levels of concentrate. a
Item Concentrate, % BW SEM Response P =
1.0 1.5 2.0
Average daily gain, lb/d 1.63 1.79 1.96 0.07 Linear < 0.05
Forage OM intake, % BW b 1.8 1.3 1.1 0.01 Linear < 0.01
a Forage organic matter intake determined on grazing calves by the use of a sustained
release bolus containing an indigestible.
Recently, we evaluated the effects of 3 different early-weaned calf management systems on
measures of calf performance and economic return. In this study (unpublished data), calves
were early weaned at approximately 70 days of age and reared in 1 of 3 management systems
for 84 days. The systems included; 1) grazing dormant winter perennial grass pasture
(Bahiagrass) with 2% body weight concentrate supplementation, 2) Drylot with concentrate
limit-fed at 3.5% body weight, or 3) Annual pasture grazing (Ryegrass) with 1% body weight
supplementation. Our findings show that although greater body weight gain can be achieved
with drylot rearing on concentrate diets, the efficiency of this gain is lacking when compared to
calves grazing high-quality pasture with supplement (Table 4). Despite the method of calf
management system adopted, each of these systems produced profitable performance results.
Beef producers adopting early weaning systems with their young cows should consider
harvesting the value of efficient feed conversions of these young calves by designing a 3 to 4
month rearing system that best fits their local resources.
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Table 4. Evaluation of management systems for the rearing of early-
weaned calves.1
Treatment1
Item Bahiagrass Drylot Ryegrass SEM
BW, lb
d 0 197 a 215
b 225
b 7.4
d 28 245 a 276
b 270
b 8.9
d 56 269 a 342
b 322
b 10.1
d 84 336 a 417
b 367
c 10.9
ADG, lb/d
d 0 – d 28 1.94 a 2.27
b 1.66
a 0.125
d 28 – d 56 0.87 a 2.36
c 1.89
b 0.141
d 56 – d 84 2.29 a 2.58
c 1.56
d 0.136
d 0 – d 84 1.69 a 2.40
b 1.70
a 0.080
Feed Intake, lb/calf daily
d 0 – d 28 4.4 a 8.8
b 2.8
c 0.13
d 28 – d 56 5.0 a 12.6
b 3.5
c 0.22
d 56 – d 84 6.0 a 12.4
b 4.2
c 0.19
d 0 – d 84 5.1 a 11.3
b 3.5
c 0.15
Economics
Feed cost, $ BW gain 2 0.59
a 0.95
b 0.41
c 0.022
Calf value, $/calf 3 481
a 565
b 525
c 10.2
Return, $/calf 4 397
a 376
b 466
c 9.6
1Calves ealy-weaned at approximately 70 days of age. 2% = calves grazing bahiagrass pastures
and supplemented with concentrate at 2% of BW (n = 5 calves/pasture; 4 pastures); Feedlot =
calves in drylot and limit-fed concentrate at 3.5% of BW (n = 5 calves/pen; 4 pens); Ryegrass =
calves grazing ryegrass pastures and supplemented with concentrate at 1.0% of BW (n = 4
calves/pasture; 4 pastures). 2Feed cost ($/calf) divided by total BW gain of each pen.
3$1.40 per lb of calf BW.
4 Return = Calf value ($/calf) - feed cost ($/calf).
In Florida, our fall-born, early-weaned calf management systems involve the establishment of
winter annual ryegrass within Calf Nurseries for the rearing of calves. Over the past 10 years,
we have grazed early-weaned calves at an average stocking rate of four to six calves/acre.
Despite both dry and wet winters this stocking rate has proven acceptable. Optimal stocking
rate should be defined as the rate which best utilizes the available forage for maximum animal
body weight gain. On non-irrigated land, this target rate is highly dependent upon the amount of
effective precipitation received during pasture establishment. Over six consecutive years, we
have found a great deal of variability among ryegrass yield and calf performance (Table 5);
however, a stocking rate of four to six calves per acre has proven to be acceptable to achieve
rates of body weight gain similar to or greater than the gain achieved by non-weaned calves of a
similar age. In each of the studies reported in Table 5, early-weaned calves were provided
supplemental concentrate feed at a rate of 1% of body weight. Although we utilize annual
ryegrass or rye-ryegrass blends in our Florida early-weaned calf nurseries, this system will not
be practical for all regions of the country. For temperate regions of the United States, other grass
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varieties should be considered. It is important to note that high-quality forage varieties that may
not be tolerant to cow grazing may work well in an early-weaned calf grazing system. Young
calves are much gentler on the pasture, consuming forage much like a deer or goat. As well,
because the calves are smaller their dry matter intake is much less than a mature cow; therefore,
moderate yielding, high-quality forages may be good candidates for use in an early-weaned calf
nursery.
In our system, a major shortcoming of the management of an early-weaned calf occurs once the
winter annual ryegrass dies out in the spring. Once early-weaned calves are moved onto
perennial, summer pastures their performance declines rapidly. Our annual ryegrass is grazed
out by early to mid-May, leaving a 100 day deficit period until the time of normal weaning
(early August). In our studies, performance of our early-weaned calves drops by an average of
25% in the summer versus winter periods. Although performance in the winter is similar among
early-and normal-weaned calves, performance in the summer period is usually inferior for the
early-weaned calf compared to those left with their dams. This decline in performance often
results in a greater overall ADG for normal-weaned compared to early-weaned calves when
calculated from January (time of early weaning) to August (time of normal weaning). We
attribute this decline in summer performance to the lesser digestibility of our summer perennial
pastures compared to the winter annual ryegrass (Figure 4). For Florida producers, these data
would support the marketing of early weaned calves in late April or early May. Historically,
calf markets are at their greatest at this time of the year. Consideration of regional variation in
forage quality, quantity, and annual trends in market value should be considered when
determining the optimal marketing time for early-weaned calves.
Table 5. Performance of early weaned calves in both winter and summer grazing seasons over
six consecutive years (average daily body weight gain ± stnd. dev.).a
Year Winter grazing b
Summer grazing b
Stocking rate, calves/acre
Winter Summer
2000 1.89 ± 0.04 1.21 ± 0.07 3.3 3.3
2001 2.08 ± 0.06 ------- 3.3 -------
2002 1.35 ± 0.07 1.31 ± 0.18 4.4 2.4
2003 1.60 ± 0.06 1.34 ± 0.06 4.0 1.2
2004 1.73 ± 0.11 1.48 ± 0.05 6.7 2.0
2005 2.15 ± 0.10 ------- 5.3 -------
Average 1.80 ± 0.07 1.34 ± 0.09 4.7 2.2 a Calves are approximately 60 to 90 days of age at the time of early weaning. All calves are
provided supplemental feed at a target rate of 1.0% of body weight during both grazing seasons.
A commercial feed (14 and 65 % CP and TDN, respectively) was utilized in 2000, 2001, 2002,
and 2003 and a commodity blend of soybean hulls and cottonseed meal (85:15) was used in
2004 and 2005. b Winter and summer grazing periods each are approximately 100 days. Winter grazing always
occurred on annual ryegrass. Ryegrass was typically fertilized twice using a complete fertilizer,
once upon emergence and again approximately 50 days into grazing. Summer grazing consisted
of established limpograss in 2000 (Arthington and Kalmbacher, 2001) and established stargrass
in all other years.
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Figure 4. Average ryegrass an stargrass quality over two consecutive seasons (2003 and 2004).
Average stocking rate = 1.6 calves/acre. Average SEM = 0.65 and 0.29, and 1.37 and 1.27 for
ryegrass and stargrass crude protein and IVOMD, respectively.
0
5
10
15
20
25
January
February
Marc
hApril
May
JuneJuly
August
40
50
60
70
80
90
January
February
Marc
hApril
May
JuneJuly
August
Crude protein, % DM basis IVOMD, % DM basis
----▲---- Ryegrass
----□---- Stargrass
Feedlot Performance of Early-Weaned Calves
Early weaning also has positive implications on the value of calves post-weaning. Researchers
from the University of Illinois (Myers et al., 1999) investigated the effect of early weaning on
carcass merit. In their studies, they reported that early weaning improved the percentage of
calves grading USDA Choice or higher by over 30% compared to normal-weaned calves. In a
comparison of weaning age (90, 150, or 210 days), they found that calves weaned at 90 days
tended to produce higher quality carcasses.
In many ranch settings, normal-weaned calves are shipped immediately after separation from
the cow. When shipped as a complete group (not commingled) these calves typically perform
well, nevertheless, buyers often discount fresh-weaned calves due to the potential for stress-
related disease. The use of early weaning, followed by growing period of 60 to 90 days,
produces calves that have recovered from the stress of weaning and understand how to eat.
Once received into the feed yard, these calves are likely to have fewer incidences of illness. In a
study conducted in collaboration with our program and North Carolina State University, we
examined the productivity of early- versus normal-weaned calves in the feedlot (Arthington et
al., 2005). In that study, early-weaned calves were lighter at the time of normal weaning (492
versus 611 lb), but gained body weight at a faster rate during the feedlot receiving period
(Figure 5). By d 28, body weight was similar (538 versus 617 lb for early- and normal-weaned
calves, respectively). Overall, early-weaned calves gained over 1 lb/d more than normal-
weaned calves (Figure 5), despite no differences in daily feed dry matter intake (Table 6).
The most striking response to early weaning in our feedlot study was the significant
improvement in feed efficiency (Table 6). We have attributed this response to a lesser
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inflammatory reaction in early- versus normal-weaned calves in response to the stressors
associated with weaning and transport. During normal stress events the early inflammatory
reaction results in the production of acute phase proteins. In our study, early-weaned calves had
a lesser acute phase protein response following transport and entry into the feedlot. Further, a
relationship between plasma acute phase protein concentrations and daily body weight gain was
observed in normal-weaned steers during the feedyard receiving period, whereas average
ceruloplasmin concentrations were negatively associated with body weight gain in normal-
weaned (P < 0.01; R2 = 0.59), but not early-weaned (P > 0.05; R
2 = 0.21) calves. Similarly,
average haptoglobin concentrations were negatively associated with body weight gain in
normal-weaned (P < 0.01; R2 = 0.40), but not early-weaned (P > 0.05; R
2 = 0.10) calves. Other
researchers have shown that feeder calf plasma haptoglobin concentrations, upon entry into the
feedlot, are positively associated with the incidence of morbidity and subsequent number of
medical treatments required (Berry et al., 2004; Carter et al., 2002).
Table 6. Effects of early- versus normal weaning age on calf feedlot performancea
Periodb Early-weaned Normal-weaned SEM
c P =
Receiving
ADG, lb/d 1.92 0.88 0.22 0.03
DMI, lb/d 12.5 11.6 0.62 0.36
G:F 0.154 0.076 0.010 0.01
Growing
ADG, lb/d 3.04 2.60 0.11 0.05
DMI, lb/d 19.4 19.6 0.77 0.84
G:F 0.157 0.133 0.006 0.06
Finishing
ADG, lb/d 3.02 2.91 0.12 0.77
DMI, lb/d 19.2 20.2 0.64 0.33
G:F 0.157 0.144 0.007 0.35
Overall
ADG, lb/d 2.71 2.76 0.24 0.82
Total BW gain, lb 650 589 20.5 0.10
Total DMI, lb 4,231 4,357 165.2 0.62
G:F 0.154 0.135 0.004 0.02 a Early-weaned calves were removed from their dams at 85 d of age. Normal-weaned calves
remained with their dams until the day of normal weaning (average age = 300 d). bReceiving diet = d 0 to 28; Growing diet = d 28 to 112; and Finishing diet = d 112 to Table
values are least square means. ADG = average daily body weight gain. cLargest SEM of least square means (n = four pens/treatment).
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Figure 5. Percent change in body weight relative to weaning weight for early- and normal-
weaned calves. Calves were shipped during the first week in August. Early-weaned calves
were weaned (early January) and retained on the ranch of origin until the time of normal
weaning. Normal weaned calves were shipped the day of weaning. (Arthington et al., 2005).
1 4 7 10 13 16 19 22 25 28-10
-5
0
5
10
15
Early weaned
Normal weaned
28 40 52 64 76 88 100 112
0
10
20
30
40
50
60
70
Day in feedyard (Receiving period) Day in feedyard (Growing period)
Ch
an
ge
in
BW
re
lati
ve
to
BW
at
no
rma
l w
ea
inin
g, %
*
*
*
*
*
*
General Healthcare of the Early-Weaned Calf
One common question related to weaning calves at this young age is health status. It is
understandable that one would be concerned with the viability of calves of this age. In fact,
ranch-derived calves at 70 to 90 days of age have a very high health status. This is related to the
passive immunity that they obtained from their mothers through colostrum. This colostrum
provides important immunity to calves of this age. In comparison, calves of normal weaning
age (6 to 8 months) have little to no remaining passive immune protection. If normal-weaned
calves are not properly vaccinated they will be more susceptible to succumbing to disease at the
time of weaning compared to 70 to 90 day old early-weaned calves. We do not recommend
vaccinating calves at the time of early weaning, as the vaccine will likely be neutralized by the
calf’s own passive immunity. Early-weaned calves should be vaccinated according to the same
schedule used for the normal-weaned calves in the herd. One exception to this rule relates to
producers that may “gather” early-weaned from multiple sources. In this situation, the producer
often does not know the health status of the herds from which the calves are sourced. Further,
the stress of transport and commingling may elicit the onset of disease. In these situations the
producer should work with their veterinarian to develop a health-care plan that will take into
consideration the balance between disease pressure and immune protection.
One important difference that we have noticed in early-weaned calves is their susceptibility to
internal parasites. We typically treat our early-weaned calves for internal parasites twice during
the 200-day grazing period. By following this management schedule, we have noticed
significant improvements in calf body weight gain following anthelmetic treatment.
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SUMMARY
Early weaning must occur prior to the start of the breeding season to gain the full
reproduction benefits associated with this management practice.
a. Calves should not be less than 50 days of age at the time of early weaning.
b. Breed yearling heifers 30 days before the mature cowherd so that the calves will be
old enough to early wean at the start of the regular breeding season in the following
year.
Early-weaned cows will voluntarily consume approximately 30% less dry matter
following early weaning. Their decrease in dry matter intake coupled with their
concurrent decrease in nutrient demands translates into a 45% increase in nutrient
efficiency of calf gain following early weaning.
Early-weaned calves grow well on high quality annual pastures such as ryegrass, when
provided supplemental grain at a rate of 1% of body weight. When high-quality pastures
are not available, early-weaned calves will require access to greater rates of a high-
quality supplemental concentrate. At the time of early weaning (50 to 90 days of age),
the crude protein requirement of the early-weaned calf diet may be as high as 20% on a
dry matter basis.
If planning to ship at the same time, vaccinate the early-weaned calves on the same
schedule as the normal-weaned calves. Calves should not be vaccinated at the time of
early weaning, as the vaccine will be neutralized by the calf’s own passive immunity.
Early-weaned calves are highly susceptible to internal parasites. Consider anthelmetic
treatment every 50 to 60 days.
In our experiences in Florida, we have been unable to maintain the high growth rate of
the early-weaned calf into the summer. Depending on the region of the country,
producers should carefully examine their pasture forage options and consider the
efficiency of moving the calf to regions closer to feeding and finishing.
When received into the feedlot at the time of normal weaning, early-weaned calves have
greater feed efficiency compared to normal-weaned contemporaries. This is an important
production response for producers to consider when evaluating retained calf ownership
opportunities.
Early-weaned calves have been shown to have carcasses of greater USDA quality score
compared to normal-weaned contemporaries. This response is likely the result of being
placed onto concentrate diets at an earlier age. Our early-weaned calves have similar
USDA carcass quality scores as normal-weaned calves when grazed on pasture until the
time of normal weaning.
REFERENCES
Arthington, J.D., and R.S. Kalmbacher. 2002. Use of ryegrass for grazing early-weaned calves
in a subtropical environment. Soil Crop Sci. Soc. Florida Proc. 61:1-4.
Arthington, J.D., and R.S. Kalmbacher. 2003. Effect of early weaning on beef cow and calf
performance in the subtropics. J. Anim. Sci. 81:1136-1141.
Arthington, J.D., and J.E. Minton. 2004. The effect of early calf weaning on feed intake, growth,
and postpartum interval in thin, Brahman-crossbred primiparous cows. Prof. Anim. Sci.
20:34-38.
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Arthington, J.D., and J.W. Spears. 2005. The effect of early weaning on feedlot performance
and measures of stress in beef calves. J. Anim. Sci. 83:933-939.
Berry, B. A., A. W. Confer, C. R. Krehbiel, D. R. Gill, R. A. Smith, and M. Montelongo. 2004.
Effects of dietary energy and starch concentrations for newly received feedlot calves:
II. Acute-phase protein response. J. Anim. Sci. 82:845-850.
Carter, J. N., G. L. Meredity, M. Montelongo, D. R. Gill, C. R. Krehbiel, M. E. Payton, and A.
W. Confer. 2002. Comparison of acute phase protein responses of cattle in naturally
acquired respiratory disease: relationships to vitamin E supplementation and
antimicrobial therapy. Am. J. Vet. Res. 63:1111-1117.
Galindo-Gonzalez, S., J. D. Arthington, J. V. Yelich, G. R. Hansen, G. C. Lamb, and A.
DeVries. 2007. Effects of cow parity on voluntary hay intake and performance
responses to early weaning of beef calves. Livest. Sci. 110:148-153.
DeRouen, S. M., and D. E. Franke. 1989. Effects of sire breed, breed type and age and weight at
breeding on calving rate and date in beef heifers first exposed at three ages. J. Anim.
Sci. 67:1128-1137.
Martin, L. C., J. S. Brinks, R. M. Bourdon, and L. V. Cundiff. 1992. Genetic effects on beef
heifer puberty and subsequent reproduction. J. Anim. Sci. 70:4006-4017.
Martins, P. G. M. A., J. D. Arthington, R. F. Cooke, C. G. Lamb, D. B. Araujo, C. A. A. Torres,
J. D. Guimaraes, and A. B. Mancio. 2012. Evaluation of beef cow and calf separation
systems to improve reproductive performance of first-calf cows. Livest. Sci. 150:74-79.
Myers, S. E., D. B. Faulkner, F. A. Ireland, and D. F. Parrett. 1999. Comparison of three
weaning ages on cow-calf performance and steer carcass traits. J. Anim. Sci. 77:300-
310.
Nunez-Dominguez, R., L. V. Cundiff, G. E. Dickerson, K. E. Gregory, and R. M. Koch. 1991.
Lifetime production of beef heifers calving first at two versus three years of age. J.
Anim. Sci. 69-3467-3479.
Rae, D. O., W. E. Kunkle, P. J. Chenoweth, R. S. Sand, and T. Tran. 1993. Relationship of
parity and body condition score to pregnancy rates in Florida beef cattle.
Theriogenology 39:1143-1152.
Rodrigues, H. D., J. E. Kinder, and L. A. Fitzpatrick. 2002. Estradiol regulation of luteinizing
hormone secretion in heifers of two breed types that reach puberty at different ages.
Biol. Reprod. 66:603-609.
Vendramini, J. M. B., L. E. Sollenberger, J. C. B. Dubeux, Jr., S. M. Interrante, R. L. Stewart,
Jr., and J. D. Arthington. 2006. Concentrate supplementation effects on forage
characteristics and performance of early weaned calves grazing rye-ryegrass pastures.
Crop Sci. 46:1595-1600.
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BH in the Rumen: The Gateway to Seeing Benefits From Fat Supplements
T. C. Jenkins
Department of Animal & Veterinary Sciences
Clemson University
Clemson, SC 29634
Corresponding author: [email protected]
SUMMARY
BH is a microbial pathway in ruminal contents designed to reduce unsaturation of
lipids found within plant matter, and is likely an evolutionary adaptation to protect the
microbial population from antimicrobial effects of unsaturated fatty acids.
The major intermediates include an array of trans-C18:1 and conjugated linoleic acid
isomers, but most published pathways have traditionally ignored the majority of minor
intermediates and present only a superficial view of BH.
Dietary lipid drives BH and the accumulation of bioactive intermediates in the rumen. Fatty
acids originate from intake of forages and grains, oilseeds, byproducts, and fat supplements.
The impacts of BH on animal performance include protection of ruminal fermentation from
antimicrobial effects of unsaturated fatty acids, loss of dietary omega fatty acids needed for
optimal reproduction and immune function, and accumulation of conjugated intermediates
with physiological activity, such as the trans-10,cis-12 isomer that inhibits mammary
lipogenesis and causes milk fat depression.
INTRODUCTION
The major accomplishment of BH (BH) in ruminal contents is to convert unsaturated fatty acids
in plant matter to more saturated endproducts that flow to the intestines. The reason the
microbial population developed the capacity for BH has been debated. Disposal of H has been
considered, but seems unlikely given that lipid BH as a H sink in the rumen is small (< 5%) in
comparison to methane and propionate production. Considering the sensitivity of many
microbial species to cytotoxic effects of unsaturated fatty acids, it seems more likely that BH
was an evolutionary adaptation to protect the microbial population from the antimicrobial
effects of double bonds. The direct addition of hydrogen to a double bond is energetically costly
and proceeds only slowly without the presence of a catalyst, as in the case of commercial
hydrogenation of oils to raise melting point. The BH pathway in the rumen overcame this
energetically unfavorable step by first forming trans double bonds that lower the energy of
activation for subsequent functioning of the reductases. Thus, a variety of trans-monoene and
conjugated dienes containing one or more trans double bonds emerged as intermediates. Over
the decades, most published accounts of BH ignored early reports of complex intermediates and
presented oversimplified pathways that included only predominant trans intermediates. Recent
work is now being directed at accounting for all possible trans-18:1 and CLA intermediates,
including identifying their physiological biopotentcy.
The impact of BH on human health and animal performance is immense. The accumulation of
the saturated fatty acids in animal tissue has had tremendous consequences on per capita
consumption of meat and milk, following continual scrutiny of saturated fatty acids for their role
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in etiology of atherosclerosis and other human health risks. In dairy cows, fat supplements can
increase energy supply to enhance lactation performance of the cow and improve profitability.
Biohydrogenation plays a role in assisting the benefits of these fat supplements by regulating the
accumulation of rumen fatty acids that are linked to carbohydrate digestion, feed intake, and
milk fat production. Likewise, BH greatly depletes the supply of essential fatty acids to
ruminant tissues, which recent studies suggests compromises reproductive performance and
immune function of the host animal in some circumstances. Notwithstanding are the potent
physiological and metabolic functions of certain BH intermediates, especially the various
conjugated linoleic acid (CLA) isomers produced. Notable effects of CLA include their anti-
carcinogenic properties and their ability to inhibit fat synthesis.
This paper will begin with a brief overview of BH and its intermediates. This will be followed
by a description of the fat sources fed to dairy cows that drive the process of BH, and how
beneficial effects of fat supplements are modulated by the pathways of BH. The paper concludes
with a discussion on regulation of BH that might enhance utilization of fat supplements by dairy
cows.
OVERVIEW OF BH
Food consumed by ruminants first passes through the largest of the four stomach compartments
or rumen, which acts like a fermentation vat. Countless numbers of bacteria, protozoa, and fungi
in the rumen ferment the feed releasing end products that are utilized by the host animal for
maintenance and growth of body tissues. The microbial population in the rumen also is
responsible for extensive transformation of dietary lipid. Lipid transformations include lipolysis
to release free fatty acids from complex plant lipids, followed by BH to convert unsaturated
fatty acids in plant matter to more saturated lipid end products.
The BH of linoleic acid in the rumen (Figure 1) begins with its conversion to CLA. In this initial
step, the number of double bonds remains the same but one of the double bonds is shifted to a
new position by microbial enzymes. Normally, the double bonds in linoleic acid are separated
by two single bonds, but in CLA, the double bonds are only separated by one single bond.
Many types of CLA are produced in the rumen of dairy cows (Bauman and Lock, 2006), but a
common CLA produced from BH of linoleic acid is cis-9, trans-11 C18:2.
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As BH progresses, double bonds in the CLA intermediates are then hydrogenated further to
trans fatty acids having only one double bond. A final hydrogenation step by the ruminal
microbes eliminates the last double bond yielding stearic acid as the final end product. Trans
double bonds only differ from cis double bonds in the placement of the hydrogens (Figure 2).
The hydrogens are located on opposite sides of the double bond for trans fatty acids, but on the
same side of the double bond for cis fatty acids. Although the difference in structure between
trans and cis fatty acids appears small, it causes significant differences in their physical and
metabolic properties.
Figure 2. Structural differences between cis and trans fatty acids.
In cows on a typical forage diet, the major trans C18:1 present in ruminal contents is trans-11
C18:1. Most of the remaining isomers have double bonds distributed equally among carbons 12
Figure 1. Major steps in the BH of linoleic and oleic acids by ruminal
microbes.
Linoleic Acid
CLA
Trans C18:1
Stearic Acid
Oleic Acid
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through 16 (Bickerstaffe et al., 1972). The exact pathways for the production of these positional
isomers are not known. Linoleic and linolenic acids are converted to several trans C18:1 and
C18:2 intermediates during BH. Mosley et al. (2002) showed that the BH of oleic acid by mixed
ruminal microorganisms involves the formation of several positional isomers of trans C18:1
rather than direct BH to form stearic acid as previously thought.
The BH process of linolenic acid in the rumen has not been researched as extensively as oleic or
linoleic acids. In most publications, linolenic acid initially is converted to cis-9 trans-11 cis-15
C18:3 by ruminal BH (Figure 3). Then, trans-11 cis-15 C18:2 was produced through the
reduction of the cis-9 double bond. This was further hydrogenated to trans-11 C18:1 to produce
stearic acid. Trans-11 cis-15 C18:2 can also hydrogenate to trans-15 or cis-15 C18:1.
Figure 3. Steps commonly reported in the BH of linolenic acid. From Kellens et al. (1986).
In a study conducted by Loor et al. (2004), linolenic acid was isomerized into three C18:3
intermediates: cis-9 trans-12 cis-15 C18:3, cis-9 trans-12 trans-15 C18:3, and trans-9 trans-12
trans-15 C18:3. Low concentrate diets (65:35 forage to concentrate) and the addition of linseed
oil in the diet increased the duodenal flow of these three C18:3 isomers. In addition, Destaillats
et al. (2005) reported that 0.3% of milk fat was the cis-9 trans-11 cis-15 C18:3 and the cis-9
trans-13 cis-15 C18:3 isomers, suggesting that these two isomers were the initial intermediates
of linolenic acid BH. Subsequently, cis-9 trans-11 cis-15 C18:3 isomer was reduced to cis-9
trans-11 C18:2 and trans-11 cis-15 C18:2, and cis-9 trans-13 cis-15 C18:3 isomer to cis-9
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trans-13 C18:2 and trans-13 cis-15 C18:2. Both cis-9 trans-11 C18:2 and trans-11 cis-15 C18:2
were able to hydrogenate to trans-11 C18:1, reducing to stearic acid. The cis-9 trans-13 C18:2
and trans-13 cis-15 C18:2 hydrogenated to trans-13 C18:1, which was then subsequently
reduced to stearic acid. They suggested that two CLA isomers (cis-9 trans-11 CLA; trans-13
cis-15 CLA) were produced from linolenic acid. However, no evidence supporting this route
was given in this study. Wąsowska et al. (2006) reported that cis-9 trans-11 cis-15 C18:3 and
trans-9 trans-11 cis-15 C18:3 were accumulated by linolenic acid BH in strained rumen fluid.
They also found that the trans-11 cis-15 C18:2 originated from linolenic acid, but cis-9 trans-11
CLA was not observed in their study.
In a recent study by Lee et al. (2011), a stable isotopic tracer study was done to investigate the
BH intermediates, including CLA, of 13
C-linolenic acid incubated in cultures of mixed ruminal
microorganisms. Results from the study showed a total of eight CLA isomers had carbons that
originated from linolenic acid. The authors pointed out that these results do not prove that
linolenic acid will yield all these CLA isomers in the live animal under all circumstances, but
only proves the capability of the anaerobic population to convert linolenic acid to CLA. The
production of CLA isomers in ruminal contents varies with the predominating microbial species,
such that changes in diet offered the animal could dictate the presence or absence of a particular
CLA isomer.
DIETARY FAT SOURCES THAT DRIVE BH
Grain and Forage Lipids
The fatty acid content of most cereal seeds and forages typically ranges from 10 to 30 g/kg DM,
with the majority of the fatty acids classified as unsaturated (predominately oleic, linoleic, and
linolenic acids). Among the unsaturated fatty acids, linolenic acid is the predominant fatty acid
in most forage species followed by linoleic acid (Hatfield et al., 2007). In the cereal seeds, fatty
acids are comprised mainly of linoleic acid followed by oleic acid.
Fatty acid concentrations in some pasture can exceed 50 g/kg DM, depending on plant species,
stage of maturity, environment, etc. Fatty acid content of annual ryegrass pasture that was
clipped in the field, immediately immersed in liquid nitrogen, and then freeze dried contained as
much as 68 g/kg DM total fatty acids (Freeman-Pounders et al., 2009). Cattle grazing some
species of immature pasture, in effect, may be consuming a high fat diet. Much lower
concentrations are usually seen in hay and silage prepared from the same plant species. This is
partially due to loss of plant leaves where chloroplast lipid is concentrated, but also due to plant
metabolism of stored energy sources. Plant enzymes can continue to function in dried forage
containing as little as 5 to 10% moisture. Plant maturity has a definite impact on both fatty acid
content and fatty acid composition. Fatty acid content (g/kg DM) generally is highest in the
spring and fall seasons and lowest in the summer months. For example, fresh perennial ryegrass
contained 32 g/kg DM total fatty acids during primary growth in May, but only 12 g/kg DM at
the beginning of second regrowth (Bauchart et al., 1984). Linolenic acid follows a similar
seasonal pattern (Bauchart et al., 1984). As linolenic acid declines over the summer months,
percentages of palmitic and linoleic acid increases.
It is not only the amount of fatty acids in grains and forages that determine BH effects in the
rumen, but also the form of the fatty acids. Information is just starting to become known about
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accumulation of free fatty acids in forages. Fatty acids in forages are usually bound to glycerol
making them less susceptible to disrupt fermentation in the rumen. Recent data are showing
increased free fatty acids in forages in some circumstances. For example, free fatty acids in
ryegrass were reported in one study to increase from 2% to as much as 73% of total fatty acids.
Also, work done at The University of Georgia at Tifton (Cooke et al., 2007) reported seeing free
fatty acids in whole cottonseed as high as 30% compared with a normal free fatty acid content
of <7%. Replacing the normal cottonseed with the high free fatty acid cottonseed reduced milk
fat from 4.2 to 3.6%.
Distillers Grains
Fermentation of corn mash produces ethanol, which is distilled to remove the ethanol and
centrifuged to remove as much excess liquid as possible. The liquid fraction can be dehydrated
to produce condensed solubles and the solid fraction may be sold directly as wet distiller’s
grains or dehydrated to produce dried distiller’s grain. The condensed soluble can be blended
with the distillers grains to produce wet distiller’s grains + soluble (WDGS) or dried distiller’s
grains + soluble (DDGS).
Table 1. Nutrient composition of corn co-products.
Nutrient WDG MDGS DDG DDGS
DM, % 25-35 50 88-90 88-90
CP, % 30-35 30-35 25-35 25-32
Fat, % 8-12 8-12 8-10 8-10
NDF, % 30-50 30-50 40-45 39-45
TDN, % 70-110 70-110 77-88 85-90
aWet distillers grain (WDG); Modified distillers grains + soluble (MDGS); Distillers
dried grains (DDG); Distillers dried grains + soluble (DDGS)
Adapted from Tjardes and Wright. (2002).
Large quantities of DDGS are now available throughout the United States as a dairy feed
ingredient due to the rapid growth of ethanol plants primarily in the Midwest. Maximum feeding
levels of DDGS in dairy diets can approach 20% or more of the feed dry matter (Schingoethe et
al., 2002). With DDGS containing 25-35% crude protein and 8-10% fat (Table 1), its inclusion
in the diet can substantially replace other protein supplements and elevate total ration fat
content. Modified distiller’s grains + solubles (MDGS) contain even higher protein (30-35%)
and fat (8-12%) concentrations. Fat concentrations in MDGS can reach 15% or higher.
Variability in the fat content of DDGS both within and across production plants is an important
consideration that should be taken into account when formulating diets.
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Oilseeds
Oilseeds contain relatively high amounts of fatty acids, but by nature of their hard outer seed
coat, might invoke less microbial shift and CLA accumulation than expected. Evidence of some
oilseed protection from ruminal BH can be seen by their ability to alter milk fatty acid
composition. Feeding whole oilseeds (i.e. whole soybeans, whole cottonseeds, whole sunflower
seeds, etc) to cows increases tissue and milk unsaturation according to some reports. When diets
containing 0, 10, 15, or 20% whole cottonseed were fed to cows, 18:1 in milk steadily increased
from 23.5 to 32.0% of total fatty acids (DePeters et al., 1985). However, there were no changes
in milk 18:2 or 18:3 as cottonseed increased in the ration. Processing of the seed can affect the
degree of protection from ruminal BH and the extent that milk fatty acids are altered. Disruption
of the seed coat exposes the oil to the microbial population and the potential for fermentation
problems and BH shifts. The seed coat can be sufficiently broken by chewing and rumination, or
through a variety of processing techniques such as extrusion or grinding. Roasting of cottonseed
was reported to reduce BH (Pires et al., 1997).
In a meta-analysis of published data examining how ruminal fatty acid losses compare among
fat sources (Jenkins and Bridges, 2007), oilseeds on average increased duodenal flow but
reduced apparent ruminal losses only for oleic acid. Oleic acid ruminal losses were lower for
oilseeds than for unprotected fats in 12 of the 15 oilseed observations. Protection by oilseeds
was not as effective for polyunsaturated fatty acids as it was for oleic acid. Only 5 of the 20
oilseed observations were below the prediction interval for linoleic acid loss as defined by the
unprotected fats. The oilseed data falling in the protected region were whole soybeans, with
lower protection reported when the seeds were processed. The remaining oilseed data points,
consisting mainly of cotton and canola seeds, fell within the prediction intervals indicating that
their responses were more similar to unprotected fats. In the case of linolenic acid, only 2 of the
15 oilseed data points had ruminal losses below the prediction interval, which came exclusively
from whole soybeans.
Fat Supplements
A useful way to classify fat supplements for dairy rations is based on their expected rumen
response. Terminology varies widely for classifying fat sources according to nutritional effects,
but most groupings consider the extent that a fat source depresses digestibility of the basal feed
ingredients and the extent that the fat source resists BH. On this basis, fats can be classified as
rumen-active, rumen-inert, or protected. The term “rumen-inert” has been assigned to fats that
were specifically designed to have little, if any, negative effect on feed digestibility when fed to
dairy cattle. Rumen-inert fats often have the added advantage of being dry fats that are easily
transported and can be mixed into the diet without the need for specialized equipment. Rumen-
inert fats are often high in calcium salts of fatty acids, saturated fatty acids, or hydrogenated
fats. Fats in this category have also been referred to as “bypass” fats.
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The “rumen-active” fats have the potential to interfere with microbial fermentation in the
rumen and reduce feed digestibility to varying degrees. Digestibility of the fibrous
carbohydrate fraction is especially susceptible to antimicrobial effects of rumen-active fats.
Generally, unsaturated fatty acids depress fiber digestibility more than saturated fatty acids.
Rumen-active fats include fats of animal origin (tallow, grease, etc), plant oils (soybean oil,
canola oil, etc), oilseeds (cottonseeds, soybeans, etc), and high fat byproducts such as residues
from food processing plants. Rumen-active fats undergo BH by ruminal microbes and
generally have little impact on modifying milk fatty acid profile.
The term “protected fat” is most applicable to fat sources specifically designed to resist BH by
ruminal microbes and modify fatty acid profile of body tissues and milk. Many of the protected
fats are based on surrounding unsaturated fatty acids by a protective capsule that acts to shield
the internal fatty acids from BH. Another strategy for protection is chemical modification of
unsaturated fatty acids to forms that resist BH, such as the conversion of fatty acids to fatty
amides.
A single fat source may overlap two, or even all three fat groups to some extent. For example, at
normal levels of supplementation, some rumen-active fats, such as tallow, are fed to dairy cows
without evidence of consistent problems with fiber digestion. Even whole oilseeds help to lessen
the severity of digestion problems by encapsulation of antimicrobial fatty acids within their hard
outer seed coat. However, classification according to ruminal digestion is better defined at high
levels of supplementation, where the frequency of digestibility problems for tallow and oilseeds
is much greater than for the rumen-inert fats. The oilseeds may also overlap as protected fats in
instances where their hard outer seed coat provides protection from BH. However, disruption of
the outer seed coat by chewing and rumination often leads to oilseeds having little ability to
enhance unsaturated fatty acids in milk.
BH REGULATION OF FAT BENEFITS
Lactation Performance
Elevating fatty acid concentration in ruminal contents may cause a number of changes in
ruminal characteristics that determine the success of the fat supplement in achieving its desired
outcome. For example, fatty acids are antimicrobial agents that can disrupt normal function of
the rumen microbial ecosystem. Disruption of fermentation is most severe for fat sources high in
unsaturated fatty acids, which inhibit growth and function of ruminal microbes more than
saturated fatty acids (Jenkins et al., 2008). Unsaturated fatty acids exert cytological damage by
adhering to the plasma membrane of microbial cells, followed by penetration into the lipid
bilayer. The fatty acids can then cause disorganization of the membrane lipid bilayer that leads
to inactivation of membrane-bound enzymes (Jenkins, 2002). An alternative explanation is the
“coating” of feed particles by lipid, which blocks the action of cellulolytic enzymes. However,
many recent studies suggest that lipid binding to feed particles protects against antimicrobial
effects of fatty acids by reducing their accumulation onto the plasma membrane of microbial
cells (Jenkins, 2002).
In addition to disruption of ruminal fermentation, fat added to dairy rations also can reduce feed
intake, which can greatly reduce or even eliminate a positive milk response. Any boost in
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energy density of the ration from added fat does little to increase energy for milk if it is
accompanied by reduced consumption of total feed. Several causes for the depression in feed
intake by added fat are under consideration. These include reduced gut motility, reduced
acceptability of diets with added fat, release of gut hormones, and oxidation of fat in the liver
(Allen, 2000). Refer to Allen (2000) for a description of each factor and a comparison of fat
sources. Gut hormones continue to receive considerable attention as regulators of food intake.
Depressed feed intake in cows fed fat supplements has been attributed to changes in
cholecystokinen (Choi and Palmquist, 1996) and glucagon-like peptide 1 (Benson and
Reynolds, 2001). Other peptides of gut origin, such as peptide YY, pancreatic glucagons,
glicentin, and oxyntomodulin, have been linked to reduced feed intake patterns in animals fed
fat (Holst, 2000). Biohydrogenation has a possible link to regulation of feed intake because
previous work has shown that abomasal infusion of unsaturated fatty acids causes greater feed
intake depression than infusion of saturated fatty acids (Drackley et al., 1992; Bremmer et al.,
1998). Dietary factors that enhance rates of BH and lessen the flow of unsaturated fatty acids to
the intestine in turn might also maintain higher feed intakes. A study by Litherland et al. (2005)
showed that the intake depression was greater following abomasal infusion of unsaturated free
fatty acids than it was following infusion of unsaturated triglycerides. Also, as intake declined in
the study by Litherland et al., (2005), the concentration of plasma glucagon-like peptide 1
increased but plasma concentration of cholecystokinen did not change.
Another connection of BH with lactation performance is diet-induced milk fat depression
(MFD), which continues to have major economic impact in the dairy industry and a priority for
finding solutions. Current thinking links MFD with CLA produced from BH by the mixed
microbial population. It was discovered that a CLA, namely the trans-10, cis-12 isomer, was
closely associated with milk fat depression. This led to the BH theory of MFD that suggested
feeding management was linked to an abnormal ruminal fermentation causing accumulation of
the trans-10, cis-12 isomer. According to a study conducted by Baumgard et al. (2000), trans-10
cis-12 CLA decreased the lipogenic rate and milk fat synthesis of dairy cows, showing a 42%
decrease in milk fat content and a 48% reduction in milk fat yield. These researchers also found
that lipogenic activity decreased 82% using a radio-labeled acetate, and the activity of acetate
oxidation to carbon dioxide was reduced to 61% in dairy cows inoculated with trans-10 cis-12
CLA. Additionally, the mRNA expression of all measured enzymes decreased from 54 to 39%
after dosing with trans-10 cis-12 CLA. The results suggested that the trans-10 cis-12 CLA
inhibited milk fat synthesis by decreasing enzyme activity through the inhibition of gene
expression affecting de novo fatty acid synthesis, uptake, and transport. Trans-9 cis-11 CLA and
cis-10 trans-12 CLA have also been reported as potential inhibitors of milk fat synthesis (Sæbø
et al., 2005; Perfield II et al., 2007) with the former being associated with a 15% reduction in
milk fat yield.
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Figure 4. The shift in intermediates produced from BH of linoleic acid in ruminal contents as a
result of a diet-induced microbial shift.
Meeting Essential Fatty Acid Demands
The -6 and -3 parent compounds (linoleic and linolenic acids, rspectively) cannot be
synthesized by body tissues and, therefore, must be supplied in the diet. Thus, linoleic and
linolenic acids are regarded as essential because they are required for normal tissue function but
cannot be synthesized by body tissues. A typical total mixed ration of grains and forages
generally contains adequate essential fatty acids to meet the needs of the animal. However, the
majority of the dietary essential fatty acids are destroyed by BH. Interest continues on finding
ways to bypass unsaturated fatty acids from BH and increase their delivery to body tissues. Part
of the interest in protecting omega fatty acids from BH is to enhance their concentration in milk
for value-added opportunities, and part is to enhance their concentration in body tissues of the
cow to enhance production and health.
Nutritional control of milk fatty acid profile continues to receive attention whether the goal is to
improve manufacturing properties of milk or to enhance the concentration of fatty acids having
beneficial health effects in humans. The key objective is usually to increase one or more
unsaturated fatty acids in milk. For instance, increasing oleic acid content in milk enhances the
plasticity and softness of milk fat, which has interested processors attempting to improve the
spreadability of butter. Also, market pressures are aimed at enhancing the concentration of the
unsaturated fatty acids in milk known to enhance human health. This has led to considerable
interest in finding ways to shield dietary unsaturated fatty acids from BH in order to enhance
their absorption and delivery to the mammary gland. Oleic acid concentration in milk fat
normally varies from 18 to 24% of total fatty acids. Various rumen-protected fats, some
commercialized and some not, pushed oleic acid in milk to as much as 48%. The effects of
protected fats on milk linoleic acid concentration have been less dramatic. Linoleic acid
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concentration in milk normally ranges from 1.5 to as much as 4% when cows are fed control
diets with no added fat. Feeding rumen-protected fats increased the upper range of linoleic acid
concentration to about 6.5%. Another significant finding bringing a great deal of attention to BH
intermediates in milk fat was the discovery that CLA had beneficial effects on human health,
most notably cancer-fighting properties. It was the cis-9, trans-11 CLA isomer in particular that
received the most attention for its anticarcinogenic properties. The recent interest in enhancing
BH intermediates in milk propagated research to determine the origin and possible enhancement
of beneficial fatty acid isomers produced in the rumen.
Reducing BH and increasing tissue delivery of unsaturated fatty acids also has improved
reproductive performance of dairy cows in some studies. Reported improvements of
reproductive performance from added fat include higher conception rates (Schneider et al.,
1988; Sklan et al., 1989; Ferguson et al., 1990), increased pregnancy rates (Schneider et al.,
1988; Sklan et al., 1991), and reduced open days (Sklan et al., 1991). Staples (2006)
summarized results from 16 published studies that reported a significant (P < 0.10) improvement
in conception rate across a wide range of fat sources. Conception rate across the 16 studies
improved from 50 to 71% when fat was fed. The mechanism of how fat supplements alter
reproductive performance is not clear, but fats as a source of essential fatty acids remains a
possibility. Supplemental omega-3 fatty acids have been proposed to enhance reproduction by
providing parent omega fatty acids for the synthesis of adequate prostaglandins involved in
reproduction. Despite strong evidence of a link between reproduction and the omega fatty acids,
questions remain regarding the proper amounts, types, and timing of feeding additional fatty
acids for maximum reproductive response. According to Staples (2006), cows showing a
positive reproductive response to added fat were being fed fat supplements at a minimum of 15
g/kg diet DM. Based on this observation, Staples (2006) suggested that fat supplementation at
15 g/kg was adequate to obtain a reproductive response. However, it is not clear as to which
fatty acids (linoleic, linolenic, DHA, EPA) or combination of fatty acids provides the maximum
response, or if levels of supplementation below 15 g/kg diet DM were sufficient.
Intermediates of BH also might influence immune responses and disease resistance in animals.
For example, CLA decreased the growth rate in chicks and rats after they were injected with
endotoxin (lipopolysaccharide; LPS). This probably was caused by release of cytokines and the
prevention of the catabolic effects (Cook et al., 1993). Miller et al. (1994) examined endotoxin-
induced growth suppression in mice fed with 0.5 % fish oil and CLA. The fish oil fed-group lost
twice as much body weight after the inoculation with endotoxin than the CLA-fed groups. These
researchers found that the CLA in the endotoxin injection inhibited anorexia (a decreased
sensation of appetite) and increased splenocyte blastogenesis, concluding that it might inhibit
arachidonic acid synthesis preventing the catabolism of tissue by removing eicosanoid
precursors. In addition, Bontempo et al. (2004) examined the effects of CLA on the
immunological variables of lactating sows and piglets fed with a 0.5 % CLA diet. They found
that CLA-fed sows exhibited increased colostrum IgG and serum leptin, and IgG and lysozyme.
Nursing piglets of CLA-fed sows also exhibited higher levels of IgG and lysozyme. As these
results show, dietary CLA enhanced the effect of immunological variables in lactating sows and
piglets.
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INFLUENTIAL FACTORS OF BH
Changes in diets offered to ruminants affect the extent of BH in the rumen. The rumen
environmental factors such as pH, soluble carbohydrates, microbial growth factors, solid
dilution rate, and fatty acids have differential effects on BH in addition to diet supply (Hungate,
1966; Church, 1969; Martin and Jenkins, 2002).
Martin and Jenkins (2002) examined continuous culture incubations at liquid dilution rates of
0.05 and 0.10/h with pH values of 5.5 and 6.5, and 0.5 and 1.0 g/L of mixed soluble
carbohydrate. They found that the major environmental factor that influenced formation of CLA
and trans-C18:1 from linoleic acid BH was culture pH. At pH of 5.5, the concentration of trans-
C18:1 and CLA were significantly reduced. Similar effects were observed by Troegeler-
Meynadier et al. (2003). They found that the amounts of BH products were always lower at pH
6.0 than at pH 7.0 at 24 h from in vitro incubations in ruminal fluid. Low amounts of CLA at pH
6.0 could be due to low isomerase activity or to high reductase activity. Moreover, they found
that low pH (pH 6.0) resulted in lower amount of trans-11 C18:1 at all incubation times
compared with higher pH (pH 7.0), but concentration of trans-10 C18:1 was higher at 16 to 24 h
of incubation. Low pH inhibited initial isomerization and the second reduction (trans-11 C18:1
to stearic acid), leading to an accumulation of trans-11 C18:1 in ruminal cultures (Troegeler-
Meynadier et al., 2006). Choi et al. (2005) reported that cis-9 trans-11 CLA are produced at pH
higher than 6.2 by rumen bacteria, but trans-10 cis-12 CLA are produced more than cis-9 trans-
11 CLA at lower pH. They concluded that trans-10 cis-12 CLA producing bacteria may be more
aero and acid-tolerant than cis-9 trans-11 CLA producing bacteria.
Oleic acid BH was also affected by ruminal pH and dilution rate. AbuGhazaleh et al. (2005)
reported that low pH and dilution rate are restricted to formation of trans-C18:1 and increased
the concentration of stearic acid from oleic acid. They conducted the experiment using 13
C-
labeled oleic acid to determine BH intermediates in mixed ruminal microorganisms grown in
continuous cultures at different pH and liquid dilution rate. At pH 6.5 and 0.10/h dilution rate, 13
C enrichment was detected in trans-6 through 16 C18:1 isomers. However, at pH 5.5 and
0.05/h dilution rate, 13
C enrichment was not detected in any trans isomers with a double bond
position over C10.
Qiu et al. (2004) reported that reduced ruminal pH can affect microbial populations, especially
cellulolytic bacteria. Total cellulolytic bacteria numbers are reduced, accompanied by reduced
acetate-to-propionate ratio and BH when pH was low. The rumen pH also influenced fungal
growth and metabolism. Culturing rumen fungi at pH 6.0 and pH 7.0 slowed BH compared pH
6.5. CLA production was increased by pH 7.0 compared to pH 6.0 and pH 6.5. Therefore,
optimum pH was 6.5 and 7.0 for BH and CLA production, respectively, by ruminal fungi (Nam
and Garnsworthy, 2007a).
Vitamins effects on BH remains a possibility but many questions remain. Pottier et al. (2006)
determined that vitamin E supplementation to cows increased milk fat content, decreased trans-
10 C18:1 concentration in milk, and increased the concentration of cis-9 trans-11 CLA and
trans-11 C18:1 in milk. Not much is known, however, what vitamin E mechanism is responsible
for the BH process. Researchers have suggested four possibilities: 1) Vitamin E might act as an
electron donor for the reduction of the cis bond of the CLA. 2) Vitamin E might be metabolized
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106
to become electron donors by ruminal microorganisms 3) Vitamin E might act as an electron
donor to restore α-tochopherolquinol and deoxy-α-tocopherolquinol. 4) Vitamin E could inhibit
the growth and function of trans-10 C18:1 producing bacteria. In a later study, Nam and
Garnsworthy (2007b) reported that the addition of VFA and vitamin E did not affect the pattern
or extent of BH by mixed ruminal fungi in in vitro cultures. Other antioxidants could also affect
BH.
Finally, the concentration of fatty acid substrates affects the BH process. Polan et al. (1964)
found that high amounts of stearic acid were produced from BH in cultures inoculated with low
concentrations of linoleic acid. As the linoleic acid concentration increased, the conversion to
stearic acid decreased. Similarly, Harfoot et al. (1973) found that linoleic acid inoculated at less
than 1.0 mg/ml of ruminal contents resulted in stearic acid being the primary end product. When
the concentration of linoleic acid increased to more than 1.0 mg/ml of ruminal contents, trans-
11 C18:1 was the primary end product. Over the years, results have shown that high amounts of
long chain fatty acids irreversibly inhibit the final BH step of C18:1 to stearic acid. Troegeler-
Meynadier et al. (200, 2006) confirmed that a high concentration of linoleic acid inhibited both
the reduction of CLA to trans-C18:1 and the reduction of trans-C18:1 to stearic acid, thus
increasing CLA concentration in the rumen. High amounts of linolenic acid, however, inhibited
linoleic acid isomerization and led to lower CLA and higher trans-11 C18:1 concentrations. Fish
oil fatty acids also influence the pattern of BH. AbuGhazaleh et al. (2002,2003) reported that
lactating dairy cows fed fish oil produced milk with higher concentrations of cis-9 trans-11
CLA and trans-11 C18:1 These changes may have been due to the inhibited reductase activity
of ruminal microorganisms, causing the accumulation of CLA and trans-C18:1. Wąsowska et
al. (2006) found that the major fatty acids in fish oil, EPA or DHA, only partially inhibited
ruminal BH.
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Why Cows Die on Dairies
SEPTEMBER 2012 1
Dairy Sessions
Moderators: Matt Dodd, Kirk Smith, Jim Bennett
Franklyn Garry,1 DVM, MS, Dipl ACVIM; Craig McConnel,
2 DVM, PhD
1Department of Clinical Sciences
Colorado State University
300 West Drake Road
Fort Collins, CO 80521 2Charles Sturt University
SAVS, Boorooma Street
Wagga Wagga, NSW 2678, Australia
ABSTRACT
On-farm death of adult dairy cows is a significant problem for both economic and animal
welfare reasons. Adult cow mortality losses on dairies have increased in recent years. These
losses and their causes are not carefully monitored or evaluated on most dairies, leaving
producers and veterinarians without the information needed to manage them. The reasons cows
die are multiple and complex, necessitating an improved approach to diagnosis, information
management and analysis.
RÉSUMÉ
La mort à la ferme de vaches laitières adultes constitue un problème important pour des raisons
à la fois économiques et de bien-être des animaux. Les pertes dues à la mortalité des vaches
adultes dans les laiteries ont augmenté au cours des dernières années. Ces pertes et leurs causes
ne font pas l’objet d’un suivi rigoureux et d’une évaluation dans la plupart des fermes laitières,
les producteurs et les vétérinaires ne disposent donc pas de l’information dont ils ont besoin
pour assurer la gestion de ces pertes. Les raisons pour lesquelles les vaches meurent sont
multiples et complexes, ce qui nécessite une meilleure approche en matière de diagnostic, de
gestion de l’information et d’analyse.
INTRODUCTION
Death losses have not been studied very intensively in the dairy industry. Yet, mortality rates in
the dairy industry are much higher than those in the cow-calf or feedlot industries. Estimates of
these death losses are variable. Unless they focus on monitoring cow deaths, dairy producers
may underestimate the amount of adult cow death loss on their operations. The SDA:APHIS:VS
National Animal Health Monitoring System (NAHMS) Dairy 2007 survey reported that 5.7% of
dairy cows die on-farm across the country each year, an increase from 4.8% of the January 2002
inventory, and 3.8% of the January 1996 inventory.14,15
Information from computerized dairy record systems suggests that mortality rates have
continually increased over the last 10 years. In some states, adult cow mortality exceeds 10%
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per year.2,4
Few formal studies have focused on this issue, yet dairy cattle death losses are an
extremely important problem. Not only are these losses an economic disaster, they also
represent very substantial problems with animal well-being.
Adult cow death loss is an issue that should be very important to producers and veterinarians.
But rising rates of occurrence across the industry suggests that veterinarians and producers do
not have the information required to manage the problem appropriately. The purpose of this
presentation is to critique the information we have, consider what information we need, and
suggest changes in information gathering for dairy herds that would help diminish losses.
WHY DO DAIRY COWS DIE?
Most studies of dairy cow mortality have come from outside the United States. Studies from the
US on this issue have been primarily focused on culling and herd turnover rates, rather than
death losses per se. The 2007 national survey of dairies in the US14 showed that approximately
23.6% of dairy cows left herds permanently during 2007, and that approximately 5.5% of these
cows were sold to other dairies, while 94% were culled (i.e. sold and not returned to milk
production, sent for slaughter). The reasons cows were culled included reproductive failure
(26.3% of culled cows), mastitis and udder problems (23%), lameness or injury (16%), other
disease (3.7%), and poor milk production not related to these other problems (16%), while other
miscellaneous reasons accounted for about 8% of culling. Therefore, on average, the
overwhelming majority of dairy cows leaving farms are not fit for sale as dairy production
animals, and approximately 50% of these cows leave because of disease or injury problems,
rather than being selectively removed because of low fertility or milk productivity.
Adult cow death losses appear to be attributable to reasons similar to those for culling cows. A
recent literature review identified 19 studies between the years 1965 and 2006 that focused on
dairy cow mortality in countries with relatively intensive dairy production.13
While 10 of
the 19 studies provided information about causes of death, none of the diagnoses were founded
on necropsy evaluation. Only a single study discriminated between cows that were euthanized or
died unassisted. The categories used to describe causes of death were relatively uniform across
studies and were presented as accidents, calving disorders, digestive disorders, locomotor
disorders, metabolic disorders, udder/teat disorders, other known reasons, and unknown reasons.
The NAHMS Dairy 2007 survey recorded causes of death similarly to those established through
the literature review, documenting the percentage of cow deaths due to euthanasia due to
lameness or injury (20.0%), mastitis (16.5%), calving problems (15.2%), respiratory problems
(11.3%), scours, diarrhea, or other digestive problems (10.4%), lack of coordination or severe
depression (1.0%), poison (0.4%), other known reasons (10.2%), and unknown reasons
(15.0%).14
Let’s consider what the preceding information means. First, it suggests that historically the
careful tracking of causes of mortality on dairies has not been seen as a high priority. Such an
attitude would make sense if deaths occur very infrequently and appear to have little to do with
the health of the remaining herd. It makes a lot less sense when 5 to 10% of standing herd
inventory is lost to death each year. This information also speaks to the diverse health
challenges seen on dairies. Dairy cows are complex animals that go through multiple life stages
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in the course of their residence on a farm. This is very different than a beef feedlot where most
of the animals are young and growing, somewhat equivalent to dairy heifers. In these
populations, infectious respiratory disease is far and away the number one health challenge that
predisposes to euthanasia and death. For adult dairy cows there is no single predominant life-
threatening disease.
It is also worth noticing that the categorization systems used on dairies and reported in the
literature are not very helpful when it comes to instituting corrective actions. For example, if
you consider the category of lameness as a cause of death, there are so many potential causes of
lameness that it would be difficult to institute a specific corrective action that would decrease
the numbers in this category. Similarly, consider the wide range of disease problems that could
be categorized as digestive death.
HOW GOOD IS OUR INFORMATION ABOUT CAUSE OF DEATH?
Cause of death entered in dairy record systems is usually based on producer assessment and
diagnosis. It appears that most dairy veterinarians are minimally involved in the diagnosis of
cause of death, and relatively few US dairy operations perform necropsies in an effort to
determine the cause of cow death. The NAHMS Dairy 2007 study reported that necropsies were
performed on only 13% of operations, and only 4.4% of cow deaths received a postmortem
examination.14
Therefore, historically almost all studies of dairy cow mortality are based on
producer assessment rather than veterinary diagnosis, and the causes of death are described
using broad categories that do not provide much information about specific cause.
Dairy record systems appear to be an unreliable source of information concerning cause of death
in individual animals. We have been studying the phenomenon of dairy cow mortality over the
last several years. Our findings suggest that dairy producer assessment of the proximate cause of
death is inaccurate approximately 50% of the time. Our results also validate that there are
multiple causes of dairy cow death.9 It seems reasonable to suggest that numerous health
problems in dairy cows are not recognized early enough or treated appropriately to promote an
optimal outcome, but this type of information cannot be retrieved from record systems.
Furthermore, without good descriptors and records of the reasons that cows die, preventive
measures that should decrease disease and death are not modified or improved to address the
problem.
No specific reason has been identified for the increase in dairy cow death rates. In conversation
with producers and veterinarians, some have questioned whether the federal regulations
regarding down dairy cows and neurologic disease may have artificially increased recorded
death rates. While this will contribute to recorded mortalities, death rates were increasing prior
to the implementation of this rule.11
Furthermore, if euthanized down cows represent more than
a small fraction of dairy mortalities, we need to ask why there are so many down cows that need
to be euthanized. Others have suggested that specific disease problems, such as hemorrhagic
bowel disease, may be increasing death rates. This could certainly be true on an individual dairy,
but the increased mortality rates across the industry exceed the incidence of any specific disease
problem.
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Any conjectures on the cause of increased mortality are difficult to validate without specific
diagnoses. Determining the cause of death would provide invaluable information for preventing
future deaths and improving herd health.7 The fact that very few dairy cow deaths are evaluated
by necropsy leaves a serious information gap in any analysis of cow mortality.
EPIDEMIOLOGICAL ASSOCIATIONS WITH DAIRY COW MORTALITY
Although record systems as they are currently designed and used are not particularly helpful in
managing adult cow death losses, they do demonstrate associations between high death rates and
herd health problems. Analyses of large data sets demonstrate that herds with high rates of
disease and culling also have higher death rates.1,3,10
More specifically, high mortality in dairy
herds is related to high rates of lameness and large proportions of cows that are removed due to
lameness or injury. Mortalities tend to occur much more frequently in the early part of lactation,
coincident with increases in other health problems.2 Death losses are related to the occurrence of
respiratory disease, diarrhea, and mastitis.10
These findings should not be surprising, as they
suggest that herds that have poor ability to control lameness, injury, and infectious disease
also have increased likelihood of cow death. It is important to recognize that these
epidemiologic associations do not inform us of specific causes, and rather show that herds with
certain types of problems also have higher rates of death. The problem for the producer and
dairy consultant lies in how to determine specific actions that decrease disease prevalence and
risk of death.
WHAT CAN BE DONE TO DECREASE DAIRY COW DEATHS?
Most decisions in a low-cost production dairy model are made with input cost as the primary
driving force, and potential negative impacts on the animals in the production system are seen as
problems that must be managed as a consequence. For example, it is common that large-scale
expansion of a dairy will capture production cost efficiencies, but often with the caveat that
expansions are accompanied by substantial problems with animal health. During the time that
large numbers of animals are being imported to the herd, it is routine that disease introduction is
occurring. Numerous animal health problems are prevalent, and even increase with time.5,16
Because there are compelling reasons for dairies to expand, there is a real need for the dairy
industry and dairy veterinarians to re-evaluate dairy management systems with a focus on
optimum animal health.
An overview of the health challenges faced by dairy cows needs to recognize that some changes
in the modern dairy industry may result in systematic problems with animal care. The labor
force on most dairies is primarily composed of low-wage workers without extensive, pre-
existing dairy cow management skills. The ability of dairy personnel to adequately identify
disease in individual animals and respond with prompt individual animal attention is limited by
the extent of their experience and training. The overwhelming majority of sick cows on dairies
are identified, diagnosed, and treated by farm workers rather than veterinarians. Poor outcomes
may be an issue of poor clinical disease management in addition to any pre-existing problems
with cow physiology.
Farm necropsy examinations should be an invaluable tool to help assess cause of adult cow
death.7 Necropsy of dead animals to assess and monitor cause of death is rarely performed on
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dairies.14
This is in sharp contrast to other intensive livestock management systems, including
poultry, swine, and feedlot enterprises where necropsy monitoring is routine. Most dairy
veterinarians focus considerable effort on dairy reproduction, or udder health and milk quality,
but little time on mortality evaluation. This presents a very significant liability to the dairy
industry, because efforts to effectively decrease mortality losses are hampered by a lack of
monitoring and information necessary to accurately assess the problem.
We believe that dairy workers could be trained to more effectively monitor death losses, and to
perform on-farm necropsy examinations in consultation with veterinarians when the veterinarian
cannot be present to perform the examination on a freshly dead carcass. We have presented this
recommendation to producer groups and produced an on-line training program for that purpose
on our website.12
Very few producers or veterinarians have pursued this approach, attesting to
the notion that monitoring actual cause of death has not been seen as a valuable pursuit.
Necropsy examinations provide good information, but we also need to develop new recording
systems that allow the necropsy results to be recorded as usable information. On their own,
necropsy diagnoses provide great detail about the specific cause of death, but do not necessarily
provide information about why that specific cause occurred. Therefore, necropsy information
needs to be combined with other historical information about the affected animals to help direct
management changes.8 Our studies suggest that more than 50% of cow death losses are
attributable to causes that could be mitigated with proper management.8
Because of the complex nature of dairy management systems a variety of causes are responsible
for high disease and mortality rates, with different rates of occurrence on different operations.
The wide range of lactational incidence risk for common diseases (milk fever: 0.03%-22.3%,
retained placenta (RP): 1.3 – 39.2%, metritis: 2.2-37.3%, ketosis: 1.3-18.3%, left-displaced
abomasum (LDA): 0.3-6.3, lameness: 1.8-30%) attests to the complexity of dairy systems.6 To
adequately address such complexity requires more accurate information about current losses,
followed by management alterations that address the underlying problems. This will require
changing the nature of information used in dairy management systems. An example of mastitis
prevalence can illustrate this point: the specific infectious organism that causes a clinical
mastitis episode can have a dramatic impact on outcome, and appropriate preventative or
therapeutic measures need to be tailored to the specific cause, e.g. gram-negative vs gram-
positive, environmental vs contagious, Escherichia coli vs Staphylococcus aureus. Assessments
and record systems that track “mastitis” without identifying other specific details provide less
information than needed to establish effective interventions. Similarly, monitoring death losses
with generic terms such as “lameness” or “mastitis” and performing this monitoring on the basis
of presumption will not allow correction of management problems that may underlie the death.
SPECIFIC RECOMMENDATIONS TO DECREASE DEATH LOSSES
We have proposed an approach to monitoring death losses that should help producers identify
management changes to improve cow health and survival.8 The first step is to identify the
magnitude of the problem on a dairy and commit to improving outcomes. Like any other
substantial management change on a dairy, if the owner or manager is not committed to change
it will not actually happen. Therefore, simple analysis of the incidence of on-farm death and an
assessment of its importance to the dairy and the well-being of the cows is critical.
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Second, we recommend performing necropsy examinations to identify specific causes of death.
This information needs to be considered along with other cow information such as preceding
health problems, treatments, and individual cow circumstances as part of a complete
postmortem evaluation. It is unrealistic to assume that 100% of all dead cows will be examined
by necropsy. Our experience suggests that routine necropsy examination is important, but that
targeting cases is useful. For animals euthanized due to obvious trauma, or where the cause of
death is obvious based on priority veterinary assessment, necropsy examination usually will not
provide much more information. Alternatively, for unexpected deaths or animals without simple
specific antemortem diagnoses, necropsy can help not only define the cause of death but also
inform farm workers about the types of problems that occur on the farm.
We have developed a conceptual model to help assign cause of death to categories that have
more meaning than those simple categories that assign cause of death to an organ system that
the owner perceives was affected by disease. Necropsy is a key tool for assigning cause of
death, if the information obtained is also matched with other animal information. Dairy workers
who are involved in animal care should be included in the discussion of the necropsy and cause
of death. The monitoring and focus on cause of death as an important component of dairy
animal monitoring increases owner and worker focus on the actions needed to prevent future
death losses.
We recommend maintaining hard copy records of each case of death. When a particular
category of death is seen to be problematic, the details of the individuals in that category can be
reviewed. As with all records, they need to be used to inform management if they are to be any
use at all. Therefore, we recommend periodic meetings between farm managers and
veterinarians to consider death losses and what can be done to improve outcomes.
More focus needs to be placed on evaluating subclinical disease problems. One of the problems
with current record systems is that health events are only entered when they are obvious and
prompt a treatment. Subclinical disease does not fit this category, and therefore information
about subclinical cow problems cannot be retrieved to be compared with assessment of death
losses. Consider for example the assessment of lameness on dairies. As noted above, high rates
of lameness are strongly associated with high rates of death losses. However, most record
systems monitor lameness only when cows receive specific treatment. It is unusual for dairies to
do routine locomotion scoring that detects cows with more modest degrees of lameness. It is
likely that management changes targeted to improving overall cow locomotion will also
improve other aspects of cow health, and ultimately lead to decreased death losses.
CONCLUSIONS
There will not be a single simple answer to the problem of high mortality on dairies. Steps
toward managing this challenge will require recognizing and defining the problem, improving
information systems to provide details necessary to take action, and monitoring appropriate
metrics that promote ongoing attention to management corrections.
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REFERENCES
1. Bascom SS, Young AJ. A summary of the reasons why farmers cull cows. J Dairy Sci
1998;81:2299-2305.
2. Dechow CD, Goodling RC. Mortality, culling by sixty days in milk, and production profiles
in high- and low-survival Pennsylvania herds. J Dairy Sci 2008;91:4630-4639.
3. Dechow CD, Smith EA, Goodling RC. The effect of management system on mortality and
other welfare indicators in Pennsylvania dairy herds. Animal Welfare 2011;20:145-158.
4. DHI Computing Services, Inc. P.O. Box 51427, Provo Utah 84605-1427, 800-453-9400.
2010.
5. Faust MA, Kinsel ML, Kirkpatrick MA. Characterizing biosecurity, health, and culling during
dairy herd expansions. J Dairy Sci 2001;84:955-965.
6. Kelton DF, Lissemore KD, Martin RE. Recommendations for recording and calculating the
incidence of selected clinical diseases of dairy cattle. J Dairy Sci 1998;81: 2502-2509.
7. Mason GL, Madden DJ. Performing the field necropsy examination. Vet Clin North Am Food
Anim Pract 2007;23:503-526.
8. McConnel CS, Garry FB, Hill AE, Lombard JE, Gould DH. Conceptual modeling of
postmortem evaluation findings to describe dairy cow deaths. J Dairy Sci 2010;93:373-
386.
9. McConnel CS, Garry FB, Lombard JE, Kidd JA, Hill AE, Gould DH. A necropsy-based
descriptive study of dairy cow deaths on a Colorado dairy. J Dairy Sci 2009;92:1954-
1962.
10. McConnel CS, Lombard JE, Wagner BA, Garry FB. Evaluation of factors associated with
increased dairy cow mortality on United States dairy operations. J Dairy Sci
2008;91:1423-32.
11. Miller RH, Kuhn MT, Norman HD, Wright JR. Death losses for lactating dairy cows in
herds enrolled in dairy herd improvement test plans. J Dairy Sci 2008;91:3710-3715.
12. Severidt JA, Madden DJ, Mason GL, Garry FB, Gould DH. 2002; Available from:
http://www.cvmbs.colostate.edu/ilm/proinfo/necropsy/notes/index.html. Integrated
Livestock Management, Colorado State University.
13. Thomsen PT, Houe H. Dairy cow mortality. A review Vet Q. 2006;28:122-129.
14. USDA. 2007. Dairy 2007, Part 1: Reference of dairy cattle health and management
practices in the United States, 2007. USDA-APHISVS, CEAH, Fort Collins, CO.
15. USDA. 2007. Dairy 2007, Part II: Changes in the US dairy cattle industry, 1991-2007.
USDA-APHIS-VS, CEAH, Fort Collins, CO.
16. Weigel KA, Palmer RW, Caraviello DZ. Investigation of factors affecting voluntary and
involuntary culling in expanding dairy herds in Wisconsin using survival analysis. J
Dairy Sci 2003;86:1482-1486.
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An Update on Hypocalcemia on Dairy Farms
G. R. Oetzel
Department of Medical Sciences
School of Veterinary Medicine
University of Wisconsin-Madison
Corresponding author: [email protected]
SUMMARY
Hypocalcemia (low blood calcium) is an important determinant of fresh cow health and
milk production.
Most second and greater lactation cows experience a transient hypocalcemia around the
time of calving.
Subclinical hypocalcemia (low blood calcium without obvious clinical signs) results in
decreased early lactation milk yield, increased risk for displaced abomasum, and reduced
fertility at first service.
Subclinical milk fever is of greater economic importance than clinical cases of milk fever
because it affects a higher proportion of cows.
Measures to control hypocalcemia include nutritional approaches and strategic treatment
with oral calcium around calving.
INTRODUCTION
Hypocalcemia is particularly amenable to strategies tailored to individual cows or targeted
groups of cows. First, a substantial proportion of cows are affected by hypocalcemia. Average
blood calcium concentrations noticeably decline in second or greater lactation cows around
calving, with the lowest concentrations occurring about 12 to 24 hours after calving (Figure 1,
Kimura et al., 2006; Goff, 2008).
A cow does not necessarily have to become recumbent (down) to be negatively affected by
hypocalcemia. With or without obvious clinical signs, hypocalcemia has been linked to a
variety of secondary problems in post-fresh cows (Goff, 2008; Oetzel, 2011). This happens
because blood calcium is essential for muscle and nerve function - particularly functions that
support skeletal muscle strength and gastro-intestinal motility. Problems in either of these areas
can trigger a cascade of negative events that ultimately reduce dry matter intake, increase
metabolic diseases, and decrease milk yield (Goff, 2008).
Subclinical hypocalcemia can be defined as low blood calcium concentrations without clinical
signs of milk fever. Subclinical hypocalcemia affects about 50% of second and greater lactation
dairy cattle fed typical pre-fresh diets. If anions are supplemented to reduce the risk for milk
fever, the percentage of hypocalcemic cows is reduced to about 15 to 25% (Oetzel, 2004).
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Figure 1.Plasma concentrations of total calcium before and after calving in mature Jersey cows
with or without clinical milk fever (Kimura et al., 2006).
Subclinical hypocalcemia is more costly than clinical milk fever because it affects a much
higher percentage of cows in the herd (Oetzel, 2011). For example, if a 2000-cow herd has a
2% annual incidence of clinical milk fever and each case of clinical milk fever costs $300
(Guard, 1996), the loss to the dairy from clinical cases is about $12,000 per year. If the same
herd has a 30% annual incidence of subclinical hypocalcemia in second and greater lactation
cows (assume 65% of cows in the herd) and each case costs $125 (an estimate that accounts for
milk yield reduction and direct costs due to increased ketosis and displaced abomasum), then the
total herd loss from subclinical hypocalcemia is about $48,750 per year. This is about 4 times
greater than the cost of the clinical cases.
A recently published, large multi-site study shows that hypocalcemia around calving is most
strongly associated with reduced milk yield (Chapinal et al., 2012) and increased risk for
displaced abomasum (Chapinal et al., 2011). These studies also demonstrated that the cutpoint
for serum total calcium is higher (about 8.5 mg/dl) than was previously assumed (see Figures 2
and 3).
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Figure 2.Effect of serum total calcium on milk yield for the first 4 DHI tests after calving.
Different cutpoints were derived for serum samples collected on weeks -1, 1, 2, and 3 after
calving. Data are from 2,365 cows in 55 Holstein herds in Canada and the US (Chapinal et al.,
2012).
Figure 3.Effect of serum total calcium on the odds for displaced abomasum after calving.
Different cutpoints were derived for serum samples collected on weeks -1, 1, 2, and 3 after
calving. Data are from 2,365 cows in 55 Holstein herds in Canada and the US (Chapinal et al.,
2011).
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CLINICAL SIGNS AND TREATMENTS FOR HYPOCALCEMIA
Clinical Signs of Hypocalcemia
Clinical signs of milk fever in dairy cattle around calving may, for convenience, be divided into
three stages. Stage I milk fever is early signs without recumbency. It may go unnoticed because
its signs are subtle and transient. Affected cattle may appear excitable, nervous, or weak. Some
may shift their weight frequently and shuffle their hind feet (Oetzel, 2011).
Some cows become hypocalcemic at times other than calving and exhibit clinical signs similar
to those described above for Stage I milk fever. Such non-parturient hypocalcemias are often
triggered by periods of unusual stress or decreased dry matter intake. This condition is most
commonly seen in cows in the first 2 to 10 days of lactation, cows that are in heat, cows with
severe digestive upsets, or cows suffering from severe (toxic) mastitis (Oetzel, 2011).
Treatment Options for Hypocalcemia
Oral calcium supplementation is the best approach for hypocalcemic cows that are still standing,
such as cows in Stage 1 hypocalcemia or who have undetected subclinical hypocalcemia
(Oetzel, 2011). A cow absorbs an effective amount of calcium into her bloodstream within
about 30 minutes of supplementation (Goff and Horst, 1993). Blood calcium concentrations are
supported for only about four to six hours afterwards (Goff and Horst, 1993; 1994) for most
forms of oral calcium supplementation.
Intravenous (IV) calcium is not recommended for treating cows that are still standing (Oetzel,
2011). Treatment with IV calcium rapidly increases blood calcium concentrations to extremely
high and potentially dangerous levels (Goff, 1999). Extremely high blood calcium
concentrations may cause fatal cardiac complications and (perhaps most importantly) shut down
the cow's own ability to mobilize the calcium she needs at this critical time (Oetzel, 2011).
Cows treated with IV calcium often suffer a hypocalcemic relapse 12 to 18 hours later (Curtis et
al., 1978; Thilsing-Hansen et al., 2002). The problems with IV calcium treatment are illustrated
in Figure 4.
Cows in Stage II milk fever are down but not flat out on their side. They exhibit moderate to
severe depression, partial paralysis, and typically lie with their head turned into their flank.
Stage III hypocalcemic cows are flat out on their side, completely paralyzed, typically bloated,
and are severely depressed (to the point of coma). They will die within a few hours without
treatment (Oetzel, 2011).
Stage II and Stage III cases of milk fever should be treated immediately with slow IV
administration of 500 ml of a 23% calcium gluconate solution. This provides 10.8 grams of
elemental calcium, which is more than sufficient to correct the cow’s entire deficit of calcium
(about 4 to 6 grams). Giving larger doses of calcium in the IV treatment has no benefit (Doze et
al., 2008). Treatment with IV calcium should be given as soon as possible, as recumbency can
quickly cause severe musculoskeletal damage.
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Figure 4.Effect of IV calcium treatment with 10.5 g of elemental calcium on serum total
calcium concentrations in a mature Jersey cow with clinical milk fever (Goff, 1999).
To reduce the risk for relapse, recumbent cows that respond favorably to IV treatment need
additional oral calcium supplementation once they are alert and able to swallow, followed by a
second oral supplement about 12 hours later (Thilsing-Hansen et al., 2002; Oetzel, 2011).
Transient hypocalcemia can occur in cows whenever they go off feed or have periods of
decreased intestinal motility (DeGaris and Lean, 2008). It can be difficult to tell which comes
first - the hypocalcemia or the gastrointestinal stasis. Whatever the case, the two problems can
positively reinforce each other. During the experimental induction of hypocalcemia (Huber et
al., 1981), ruminal contractions ceased well before the onset of clinical signs of milk fever. Off-
feed cows, particularly in early lactation, are very likely to benefit from prompt oral calcium
supplementation.
Oral Calcium Supplementation Strategies
Even herds with successful anionic salts programs and minimal clinical cases of milk fever will
benefit from strategic use of oral calcium supplements (Oetzel and Miller, 2012). Start by
supplementing all standing cows who have clinical signs of hypocalcemia and all down cows
following successful IV treatment. For herds with a high incidence of hypocalcemia, it may
also be economically beneficial to strategically supplement all fresh cows with oral calcium.
Finally, cows with high milk yield in the previous lactation (>105% of herd average ME milk
production) and lame cows have the best response to oral calcium supplementation (Oetzel and
Miller, 2012). These cows gave 6.8 lbs more milk at first DHI test compared to
unsupplemented cows.
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The source of calcium in an oral supplement and its physical form greatly influence calcium
absorption and blood calcium responses. A series of experiments has shown that calcium
chloride has the greatest ability to support blood calcium concentrations (Goff and Horst, 1993;
1994). This can be explained by its high calcium bioavailability and its ability to invoke an
acidic response in the cow, which causes her to mobilize more of her own calcium stores.
Providing a typical amount of elemental calcium chloride (e.g., 50 grams of elemental calcium)
in a small oral dose (e.g., 250 ml water) provided the best absorption (Figure 5). Administering
100 grams of elemental calcium from calcium chloride in water resulted in an excessive increase
in blood calcium concentrations - perhaps enough to shut down the cow’s own calcium
homeostatic mechanisms and to invoke a calcitonin response to protect her from hypercalcemia.
Figure 5.Effect of two different doses of oral calcium chloride on plasma total calcium
concentrations, expressed as percent of baseline values (Goff and Horst, 1993).
The risk of aspiration is great when thin liquids are given orally, and calcium chloride is very
caustic to upper respiratory tissues. Calcium propionate is more slowly absorbed (presumably
because it is not acidogenic) and must be given at higher doses of elemental calcium (usually 75
to 125 grams - see Figure 6). Calcium propionate has the property of being glucogenic as well
as providing supplemental calcium.
Calcium carbonate in water did not increase blood calcium concentrations at all (see Figure 7,
Goff and Horst, 1993). This may be explained by its poorer bioavailability and by the
alkalogenic response it can invoke.
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Figure 6.Effect of oral calcium chloride and oral calcium propionate on plasma total calcium
concentrations, expressed as percent of baseline values (Goff and Horst, 1993; 1994) (Goff and
Horst, 1993, 1994).
Figure 7. Effect of oral calcium chloride and oral calcium carbonate on plasma total calcium
concentrations, expressed as percent of baseline values (Goff and Horst, 1993).
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A combination of calcium chloride and calcium sulfate delivered in a fat-coated bolus
(Bovikalc®, Boehringer Ingelheim Vetmedica, St. Joseph, MO) resulted in more sustained
improvements in blood calcium concentrations (see Figure 8) than were observed in previous
studies with oral calcium chloride or calcium propionate in water (Sampson et al., 2009). This
encapsulated version of calcium salts had the advantages of not having an unpleasant taste to the
cow, having little to no waste of the oral formulation, no risk for aspiration pneumonia, and a
more prolonged release of the oral calcium (Pehrson and Jonsson, 1991). These workers
reported a 4-fold reduction in the odds for developing clinical milk fever in cows that were
supplemented with 4 boluses around calving (Pehrson and Jonsson, 1991).
Figure 8.Effect of administration of two Bovikalc boluses on blood ionized calcium
concentrations (expressed as percent of baseline) at calving and 12 hours later. Experimental
animals were Holstein cows (n=20) with hypocalcemia at calving (Sampson et al., 2009).
Subcutaneous Calcium Treatment
Subcutaneous calcium can be used to support blood calcium concentrations around calving, but
has substantial limitations (Goff, 1999). Absorption of calcium from subcutaneous
administration requires adequate peripheral perfusion. It may be ineffective in cows that are
severely hypocalcemic or dehydrated. Subcutaneous calcium injections are irritating and can
cause tissue necrosis; administration should be limited to no more than 75 ml of a 23% calcium
gluconate solution (about 1.5 g elemental calcium) per site. Calcium solutions that also contain
glucose should not be given subcutaneously. Glucose is very poorly absorbed when given by
this route. Abscessation and tissue sloughing may result when glucose is given subcutaneously.
The kinetics of subcutaneously administered calcium indicate that it is well-absorbed initially,
but that blood concentrations fall back to baseline values in about 6 hours (see Figure 9, Goff,
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1999). Thus, repeat doses would be necessary to equal the sustained blood calcium support that
is possible with oral calcium boluses.
Figure 9. Effect of subcutaneous administration of 500 ml of 23% calcium gluconate on plasma
total calcium, expressed as percent of baseline. The 500 ml solution was divided into 10
different sites (Goff, 1999).
Timing of Oral Calcium Supplementation Relative to Calving
Strategies for giving oral calcium supplements around calving should include at least two doses;
one at calving calving and a second dose the next day. The expected nadir in blood calcium
concentrations occurs between 12 and 24 hours after calving (Goff, 1999; Sampson et al., 2009).
Giving only one oral calcium supplement around calving time leaves the cow without support
when her blood calcium concentrations are naturally the lowest. It is interesting to note that the
original protocols for oral calcium supplementation called for 4 doses - one about 12 hours
before calving, one at calving, one 12 hours post-calving, and one 24 hours post-calving. It was
very difficult to predict when at cow was in fact about 12 hours from expected calving, and
many cows calved without receiving this dose (Oetzel, 1996). The dose at calving is not
practically challenging to administer, and providing a dose sometime the day after calving will
provide critical support around the time of nadir and can still be practical in large dairies where
the post-fresh pen is locked up just once daily.
CONCLUSIONS
New research information has refined and updated our understanding of hypocalcemia on dairy
farms. We now have a better understanding of the prevalence and impact of hypocalcemia
(particularly subclinical hypocalcemia) on fresh cow performance. Strategic oral
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supplementation can mitigate the impacts of hypocalcemia, provided the oral supplements are in
the correct form and are administered at the proper time.
REFERENCES
Chapinal, N., M. Carson, T. F. Duffield, M. Capel, S. Godden, M. Overton, J. E. Santos, and S.
J. LeBlanc. 2011. The association of serum metabolites with clinical disease during the
transition period. J. Dairy Sci. 94:4897-4903.
Chapinal, N., M. E. Carson, S. J. LeBlanc, K. E. Leslie, S. Godden, M. Capel, J. E. Santos, M.
W. Overton, and T. F. Duffield. 2012. The association of serum metabolites in the
transition period with milk production and early-lactation reproductive performance. J.
Dairy Sci. 95:1301-1309.
Curtis, R. A., J. F. Cote, M. C. McLennan, J. F. Smart, and R. C. Rowe. 1978. Relationship of
methods of treatment to relapse rate and serum levels of calcium and phosphorous in
parturient hypocalcaemia. Can. Vet. J. 19:155-158.
DeGaris, P. J., and I. J. Lean. 2008. Milk fever in dairy cows: A review of pathophysiology and
control principles. Vet. J. 176:58-69.
Doze, J. G., R. Donders, and J. H. van der Kolk. 2008. Effects of intravenous administration of
two volumes of calcium solution on plasma ionized calcium concentration and recovery
from naturally occurring hypocalcemia in lactating dairy cows. Am. J. Vet. Res. 69:1346-
1350.
Goff, J. P. 1999. Treatment of calcium, phosphorus, and magnesium balance disorders. Vet.
Clin. North Am. Food Anim. Pract. 15:619-639.
Goff, J. P. 2008. The monitoring, prevention, and treatment of milk fever and subclinical
hypocalcemia in dairy cows. Vet. J. 176:50-57.
Goff, J. P., and R. L. Horst. 1993. Oral administration of calcium salts for treatment of
hypocalcemia in cattle. J. Dairy Sci. 76:101-108.
Goff, J. P., and R. L. Horst. 1994. Calcium salts for treating hypocalcemia: Carrier effects, acid-
base balance, and oral versus rectal administration. J. Dairy Sci. 77:1451-1456.
Guard, C. L. 1996. Fresh cow problems are costly; culling hurts the most. Hoard's Dairyman
141:8.
Huber, T. L., R. C. Wilson, A. J. Stattleman, and D. D. Goetsch. 1981. Effect of hypocalcemia
on motility of the ruminant stomach. Am. J. Vet. Res. 42:1488-1490.
Kimura, K., T. A. Reinhardt, and J. P. Goff. 2006. Parturition and hypocalcemia blunts calcium
signals in immune cells of dairy cattle. J. Dairy Sci. 89:2588-2595.
Oetzel, G. R. 1996. Effect of calcium chloride gel treatment in dairy cows on incidence of
periparturient diseases. J. Am. Vet. Med. Assoc. 209:958-961.
Oetzel, G. R. 2004. Monitoring and testing dairy herds for metabolic disease. Vet. Clin. North
Am. Food Anim. Pract. 20:651-674.
Oetzel, G. R. 2011. Non-infectious diseases: Milk fever. Pages 239-245 in Encyclopedia of
Dairy Sciences. Vol. 2. J. W. Fuquay and P. L. H. McSweeney, ed. Academic Press, San
Diego.
Oetzel, G. R., and B. E. Miller. 2012. Effect of oral calcium bolus supplementation on early
lactation health and milk yield in commercial dairy herds. J. Dairy Sci. 95:7051-7065.
Pehrson, B., and M. Jonsson. 1991. Prevention of milk fever by oral administration of
encapsulated Ca-salts. Bov. Pract. 26:36-37.
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Sampson, J. D., J. N. Spain, C. Jones, and L. Carstensen. 2009. Effects of calcium chloride and
calcium sulfate in an oral bolus given as a supplement to postpartum dairy cows. Vet.
Ther. 10:131-139.
Thilsing-Hansen, T., R. J. Jørgensen, and S. Østergaard. 2002. Milk fever control principles: A
review. Acta Vet. Scand. 43:1-19.
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Performance of Calves in Different Calf Feeding Systems Mark Hill, Gale Bateman, II, Jim Quigley, Jim Aldrich, and Rick Schlotterbeck
Nurture Research Center, Provimi North America, Brookville, OH 45309
Corresponding author: [email protected]
SUMMARY
A large percentage of US dairy calves are fed approximately 1 lb of milk or milk replacer
(MR) solids (i.e. 1 gallon) daily.
Calf growth in the first month of life can be increased by feeding calves approximately
twice this liquid rate but delays intake of starter and may reduce growth in the weeks
around weaning unless the liquid is gradually reduced over approximately 3 weeks to allow
rumen development.
Intermediate amounts (i.e. 1.5 gallons) of liquid diets are easy to manage and less apt to
interfere with starter intake or weaning growth.
Nutrient densities of the liquid diet for optimal growth differ depending upon amount of
liquid fed. For example, a MR fed at 1.5 to 2 lb (1.5 to 2 gallons) should have a greater CP
concentration than a MR fed at 1 lb (1 gallon).
Balancing diets correctly to not over-feed or underfeed nutrients typically reduced the cost
of body weight gain and with some nutrients and situations the reduced costs are
substantial.
INTRODUCTION
A large percentage of US dairy calves are fed approximately 1 lb of milk or MR solids (i.e. 1
gallon) daily. The number of operations feeding more than this amount of milk or MR solids
has increased over the last 10 plus years (USDA, 2012) much because of research from Dr.
Mike Van Amburgh’s laboratory at Cornell University (Diaz et al., 2001). This has not been
without controversy as to what was nutritionally correct, economical, or humanely appropriate.
Some in the industry would suggest that marketing and opinion has driven the increase in milk
or MR fed. Nonetheless, it has been a great challenge for the industry to consider how calves
are fed.
This paper and presentation will review the published literature from the last 10 to 15 years on
dairy calf feeding programs for calves less than approximately 4 months of age. Strengths,
weaknesses, and nutrients provided with different feeding programs will be mentioned and
based on published research trials.
CONVENTIONAL PROGRAMS
Two quarts of milk or reconstituted MR per feeding has been popular for over 40 years in the
US. Conventional MR are typically 22 to 24% CP (DM basis; 20 to 22% CP as-fed basis) and
22% fat (DM basis). Milk is typically 25 to 28% CP and even higher in fat (DM basis).
Feeding 1 lb of a 22% CP and 22% fat MR provides sufficient ME and CP for maintenance and
limited body weight gain (approximately 0.4 lb/day) under thermoneutral conditions. This low
feeding rate promotes an early appetite for starter feed and allows weaning as early as 28 days
of age. Indeed, early weaning programs developed in the 1950’s and 1960’s were predicated on
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limited MR, early and aggressive intake of starter and early weaning. One important feature of
early weaning programs was lower cost, since saleable milk or MR is expensive compared to
dry starter. Additionally, labor costs associated with feeding and managing calves in individual
housing fed a liquid diet are high compared to older weaned calves in group housing fed a dry
starter (Tozer and Heinrichs, 2001).
Most calves are raised in individual pens or hutches. Numerous studies have shown that
reducing or eliminating calf-to-calf contact prior to weaning reduces predisposition to disease,
improves health and growth of calves. Individual plastic hutches that are positioned to eliminate
calf contact are very effective in reducing disease transmission as long as basic biosecurity
procedures are followed. See a review of individual housing research by Quigley (2001) for
this and more information. Calf pens in barns may use solid or wire panels to separate calves.
Solid petitions, while eliminating calf-to-calf contact may compromise ventilation within the
barn. See the recent paper of Hill et al. (2011a) for a partial review of these data. Recent un-
reviewed data suggest that single or small group housing does not affect markers of immunity
(Hulbert et al., 2012abc).
INTENSIVE FEEDING PROGRAMS
As more milk or MR is fed pre-weaning, ADG increases (Jasper and Weary, 2002; Cowles et
al., 2006; Hill et al., 2006ab, 2007d). The amount of increased ADG is a function of the
nutrients provided and will be addressed in a subsequent section. However, when the amount of
milk or MR fed is more than approximately 1.5 lb DM, post-weaning ADG will be
compromised compared to calves that are hand-fed greater amounts of milk (Bar-Peled et al.,
1997; Jasper and Weary, 2002), hand-fed non-acidified MR (Cowles et al., 2006; Hill et al.,
2006ab, 2007d), or allowed free-choice access to acidified MR (Nocek and Braund, 1986;
Hepola et al., 2008). Two laboratories have measured total tract apparent DM digestion post-
weaning in calves fed low or high amounts of MR and both reported 6 to 9% lower digestion in
calves fed the high level of MR (Terre et al., 2006, 2007; Hill et al., 2010). The low digestion in
calves fed high levels of MR was associated with less development of the rumen (Terre et al.,
2006, 2007; Suarez-Mena et al, 2011). So the conundrum is how to feed more milk or MR and
maintain the increased body weight after the calf transitions to starter. One option is to not feed
more than about 1.5 lb DM per day via the liquid diet. Another approach is to gradually wean
calves over 14 to 25 days (Khan et al., 2007; Hill et al., 2007d, 2012b; Sweeney et al., 2010).
Gradual reduction of the liquid diet forces the calf to find energy from other sources, including
the starter. The calf requires about 14 days for the rumen to adapt to increasing starter intake, so
gradual weaning from high volumes of liquid require 2 weeks or more.
We assembled data from 10 peer-reviewed studies at 6 different laboratories where a
conventional (control) MR was fed along with one or more intensified MR treatments (Table 1).
A simple covariate analysis was conducted. Note the moderate and intensive MR treatments
were 26.5% and 29% CP, respectively, compared to 21.4% for calves fed the control treatments.
Calves fed the moderate rate of MR gained 29% better and calves fed the intensive treatments
gained 41% better than calves fed the control milk replacer treatments during the pre-weaning
period. Starter intake of calves fed the intensive treatment were 67% of the calves fed the
control. Feed efficiency (gain to feed) of calves fed the intensive treatment were 29% better
than calves fed the control. Starter intake and feed efficiency of calves fed the moderate
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treatment were 4% less and 9% better than the calves fed the control. However, during post-
weaning periods calves fed the intensive treatments gained less weight than calves fed the
control and calves the moderate treatment gained more weight than calves fed the control.
Overall (115 total days) calves fed the moderate and intensive treatments gained 12% and 6%
better, respectively, the rate of calves fed the control (Table 2). These studies in this database,
individually, and when combined make a compelling case that feeding more than approximately
1 lb of solids from milk or MR has merit for improving early life growth in calves. However,
they also clearly point to issues with feeding over 1.5 lb of solids from milk or MR.
Table 1. Average milk replacer composition, intake, and pre-weaning performance from
10 peer-reviewed studies where a conventional milk replacer was fed along with
a moderate and/or intensive milk replacer.
Item Control Moderate Intensive
Days 44.1 41.1 45.9
MR intake, lb/day 1.06 1.54 1.98
MR CP, % 21.4% 26.5% 29.0%
MR fat, % 20.4% 16.9% 17.8%
Starter intake, lb/day 1.34 1.28 0.90
ADG, lb/day 1.08 1.39 1.52
Gain/Feed 0.450 0.493 0.528
References: Cowles et al., 2006; Hill et al., 2006b; Raeth-Knight et al., 2009; Hill et al., 2010;
Davis Rinker et al., 2010; Stamey et al., 2012; Osorio et al., 2013.
Table 2. Intake, body weight gain, and feed efficiency from 10 peer-reviewed studies where a
convention milk replacer was fed along with a moderate and/or intensive milk
replacer (total days = 115.6).
Item Control Moderate Intensive
MR, lb DM 47 63 91
Dry feed DM, lb 546 617 535
Body weight gain, lb 212 239 226
Gain/Feed 0.357 0.351 0.361
References: Cowles et al., 2006; Hill et al., 2006b; Raeth-Knight et al., 2009; Hill et al., 2010;
Davis Rinker et al., 2010; Stamey et al., 2012; Osorio et al., 2013.
IMPACT OF SPECIFIC NUTRIENTS
The optimum protein to energy ratio for ADG in calves fed only MR has been estimated to be
approximately 48 g CP/Mcal ME in 2 trials (Bartlett et al., 2005; Blome et al., 2003). A similar
estimate was made by Donnelly and Hutton (1976) in calves fed only MR. Calves in the MR
only trials were over 2 weeks of age when the trials began and were managed in conditions
close to thermoneutrality, which may have influenced the results. Hill et al. (2009b) estimated
optimum CP:ME ratio in calves fed starter and MR at 2 rates to achieve different ME intakes.
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Optimum protein to energy ratios were 52 (low ME intake) and 55 (high ME intake) g CP/Mcal
ME. Calves in these trials were 2 to 3 days of age when the trials began and were housed in a
nursery mostly below thermoneutrality on straw bedding. Also, calves were vaccinated and
dehorned during the trial. These trials demonstrate the need for more than 22% CP (DM basis)
in MR fed at rates over the conventional rate fed in the U.S. (approximately 1 lb DM from
MR/calf day). This has also been shown in MR program trials where calves were fed both MR
and starter (Hill et al., 2006ab).
Increased fat and ME intake from MR has frequently resulted in either no change or reduced
ADG, protein accretion, and measures of structural growth (Bascom et al., 2007; Van den
Borne, 2007; Hill et al., 2009cd). Hill et al. (2009c) reported reduced digestion of most
nutrients as fat increased from 14 to 23% in 27% CP MR in a trial conducted in winter months
with ambient temperatures well below thermoneutrality. While milk is typically high in fat, MR
does not have to be formulated that way. Milk replacers that fall in the range of optimum
protein to energy ratios, as discussed above, are approximately 25 to 27% CP and 16 to 17% fat
(each DM basis; Tikofsky et al., 2001; Bascom et al., 2007; Hill et al., 2009b). Yet most MR
contain 20% fat whether conventional or intensive (22 to 29% CP) and therefore have a lower
than optimum CP to energy ratio.
Milk replacers for calves in the US are typically formulated with animal fat and are relatively
low in butyric acid, medium chain fatty acids, and linolenic acid. Additionally, calf starters and
growers are relatively low in these fatty acids. In research where these fatty acids were
supplemented to calves, ADG, hip width growth, and feed efficiency were increased
approximately 7+% and days with abnormally loose feces were reduced (Hill et al., 2007bce,
2009a, 2011ab; Fokkink et al., 2009). Additionally, calves supplemented with butyric, medium
chain, and linolenic have improved markers of both short and long term immunity (Hill et al.
2011bc).
Recent estimates of amino acid requirements have been made in 11 trials with calves fed both
starter and MR (Hill et al. 2007c, 2008a, 2011d). The benefit from balancing MR for amino
acids vs. CP was approximately 9% more ADG and feed efficiency in calves fed 22% CP (DM
basis) MR at 1 lb DM/day and over 15% for calves fed high protein MR (> 25% CP) at 1.5 lb
DM/day.
IMPORTANCE OF STARTER INTAKE
Equations from the Dairy NRC (2001) suggest that energy limits ADG in typical dry diets fed to
weaned calves. As forage is increased in the weaned calf’s diet, energy becomes more limiting
compared to diets containing no or low forage. Recent publications from different labs each
using over 900 calves report that ADG of the dairy calf between birth and 2 mo of age is
positively related to starter intake (Heinrichs and Heinrichs, 2011; Bateman et al., 2012). The
analysis of Bateman et al. (2012) was very dynamic across many feeding rates, compositions of
MR programs, and seasons of the year.
Starter intake is affected by many factors, including particle size of the diet (Lassiter et al.,
1955; Gardner, 1967; Kertz et al., 1979; Bateman et al., 2009), roughage concentration and
amount fed (Warner et al., 1956; Stobo et al., 1966; Jahn and Chandler, 1976; Porter et al.,
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2007; Hill et al., 2008b, 2009e), amount of milk (Bar-Peled et al., 1997; Jasper and Weary,
2002) or MR fed (Kertz et al., 1976; Terre et al., 2006, 2007; Suarez-Mena at al., 2011; Stamey
et al., 2012), and weaning program utilized (Hill et al.,2007d, 2012b; Kahn et al., 2007;
Sweeney et al., 2010). Because so many factors impact starter intake, and because starter intake
is positively related to growth of dairy calves (Heinrichs and Heinrichs, 2011; Bateman et al.,
2012), it is important to design feeding programs and diets to maximize starter intake in the
transition calf.
Few new papers have addressed CP requirements of the calf during the transition to dry feed.
Optimum concentrations of CP for starters fed to calves on conventional milk and MR programs
from birth to shortly after weaning were19 to 20% CP (DM basis; Lucini et al., 1991; Akayezu
et al., 1994) which is similar to the Dairy NRC (2001). Calves fed conventional milk or MR at
approximately 1 lb DM/day or MR (> 25% CP) at > 1.5 lb DM/day had optimum ADG with
starters containing 20.5% CP (63 g CP/Mcal ME; Hill et al., 2007a, 2008c; Stamey et al., 2012).
The optimum CP in starters for weaned calves from 2 to 4 mo of age was 17% (to maximize
ADG) to 18% (to maximize feed efficiency; 52 to 56 g CP/Mcal ME: Hill et al., 2008c).
GROUP HOUSING PROGRAMS
Group housing of calves is an area of interest in North America. Most of the interest has been in
eastern Canada, New York, and New England states. Several researchers have evaluated the
effect of ad libitum MR feeding on intake and growth of calves (Thickett et al., 1983; Nocek
and Braund, 1986; Fallon and Harte, 1988; Richard et al., 1988; Hepola et al., 2008; Hill et al.,
2013). Where post-weaning measurements were made (Nocek and Braund, 1986; Hill et al.,
2013), calves fed the ad libitum plane of nutrition had greater ADG pre-weaning, but less ADG
post-weaning compared to calves fed conventionally (approximately 1 lb DM/day) in individual
pens. Patterns in MR intake, starter intake, and growth in ad libitum group-housed systems
were similar to calves hand-fed intensive MR in individual housing. Hill et al. (2013) reported
when calves were fed MR ad libitum, they consumed over 95% of the MR between 6 to 8 AM
and 4 to 6 PM and standing behavior was not greatly altered compared to calves fed hand-fed
1.5 lb DM of MR/day.
INTRINSIC BENEFITS OF ENHANCED NUTRITION
There are 7 peer-reviewed trials comparing 2 or more levels of milk or MR nutrition on the
impact of future milk production (Bar-Peled et al., 1997; Shamay et al., 2005; Morrison et al.,
2009; Raeth-Knight et al., 2009; Terre et al., 2009; Moallem et al., 2010; Davis Rincker et al.,
2011). Only 2 of these trials report significant increases in milk production because of enhanced
nutrition (Shamay et al., 2005; Moallem et al., 2010). Those trials both compared an inferior
MR program to milk. Four of the 5 other trials reported trends for improved milk yield. More
details for these trials were summarized by Heinrichs and Jones (2011) along with some non
peer-reviewed trials. We gathered the treatment means from the 7 peer-reviewed trials and used
them in regression analysis. There were no statistically significant or biologically meaningful
relationships between amount of fat or protein fed to the calves and future milk fat or milk
protein yield. However, there was a significant relationship between pre-weaning ADG and
future milk yield.
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Van Amburgh (2012) performed a meta-analysis on a similar set of peer-reviewed trials but also
included several non-reviewed trials. He reported a positive relationship between feeding calves
more nutrients from milk or MR and future milk production, as well as, a positive relationship
with increased pre-weaning ADG and future milk.
There are 3 additional peer-reviewed studies correlating calf ADG on future milk production.
Each took very different approaches to collecting data and the statistical analysis and because of
these differences, creates concerns when attempting to group their results with those of the other
7 studies used in our statistical analysis. Bach and Ahedo (2008) correlated calf ADG to future
milk from a calf ranch in Spain with 900 heifers and found no statistical relationship. In this
analysis, calf ADG varied from 0.8 to 2.5 lb/day. Heinrichs and Heinrichs (2011) collected
farm data from a county in PA, USA over several years. The data set comprised over 900
animals. Starter intake during the first 2 months of life was positively correlated with calf ADG
during the first 2 months of life and future milk production. Amount of milk or MR fed did not
correlate to future milk yield. This data set was predominately calves fed approximately 1 lb of
DM from milk or a conventional MR. Soberon et al. (2012) collected data (approximately 1,800
animals) from the Cornell University herd and a nearby commercial herd. The university calves
were fed either a 28% CP, 15% fat MR powder or a 28% CP, 20% fat MR powder at
approximately 2 to 2.2 lb DM per calf daily. The commercial farm calves were fed a 28% CP,
15% fat MR powder at approximately 1.9 lb DM per calf daily. The amount of MR fed at each
site was fixed and not varied to change calf ADG. Even though the amount of MR was fixed,
calf ADG varied from 0.2 to 3.5 lb/day. Calf ADG was positively correlated with future milk
production. This paper did not describe several key factors that could relate calf ADG
differences to future milk such as starter intake and colostrum consumption (or immunoglobulin
absorption) of the calves. However, the final relationship was for 1,541 lb more milk in the first
lactation per increase in pre-weaning ADG by 1 lb (a linear relationship).
Several laboratories have compared feeding calves conventional MR at approximately 1 lb DM
daily to high 29% CP MR at approximately 2 lb DM daily and measured markers of innate
immunity. Few if any differences in innate immunity between the 2 programs were observed
and the few differences were post-weaning (Nonnecke et al., 2003; Foote et al., 2005, 2007;
Hengest et al., 2012; Ballou, 2012). We are not aware of trials that have reported reductions in
digestive or respiratory sickness using intensive or moderately intensive milk or MR programs
compared to conventional programs, however some report more sickness with intensive
programs (Cowles et al., 2006; Hill et al., 2006a; Quigley et al., 2006; Hengest et al., 2012).
During periods of cold or heat stress the maintenance requirement of calves increase (NRC,
2001). Housing situations where the bedding does not insulate the calf (i.e. concrete, metal,
wood, rock, sand, shavings, or any type of wet bedding) increase the maintenance requirements
of the calves in cool and cold weather. Housing and bedding management ameliorates cold
stress to a significant degree (Hill et al., 2007d, 2011a, 2012a). Bateman et al. (2011) conducted
a meta-analysis of 20 trials across many feeding rates, compositions of MR programs, and
seasons of the year with ambient temperatures in the unheated nursery ranging from near 0 to
100 °F (average trial temperatures ranged from 22 to 78 °F). In this meta analysis, calf ADG
increased as ambient temperature decreased. Heat stress appears harder to ameliorate than cold
stress with cooling using fans reported to reduce panting and increase ADG during summer heat
stress (Hill et al., 2011a, 2012a). Moderate increases of (25 to 50%) in the amount of milk or
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MR fed when using conventional programs feeding 1 lb of DM to 1.25 to 1.5 lb of DM are
justified in extreme cold or heat stress (Hill et al., 2007d, 2011a, 2012a). However,
management of environment with insulating, dry bedding and draft (wind) protection are critical
to the calf before more calories are fed (Hill et al., 2007d).
ECONOMIC CONSIDERATIONS
Costs can be applied to the performance summary of the 10 trial summary in Table 2 to partially
access the economics of MR feeding rate programs. In this example, costs of $1.00/lb for
control MR, $1.18/lb for moderate MR, $1.24/lb for intensive MR, and $0.23/lb for dry feed
were used. Total feed costs and cost per lb of body weight gain were lowest for the control
($171/calf, $0.81/lb), intermediate from the moderate program ($215/calf, $0.90/lb), and highest
($234/calf, $1.04/lb) for the intensive program.
Other economic considerations could be based on the value of body weight gain and calculate
the value of body weight gain over the total feed cost. Medical and health associated costs
should be similar among feeding programs, possibly higher with intensive vs. moderately
intensive or control programs (Cowles et al., 2006; Hill et al., 2006a; Quigley et al., 2006;
Hengest et al., 2012). The economics of waste milk would be different since the cost of waste
milk is presumed less than MR.
The intrinsic values less certain to estimate are future milk, less days to first calving, or the
ability of larger calves to compete as heifers. Prorating the 1,541 lb of increased milk in the first
lactation per 1 lb of ADG estimated by Soberon et al. (2012) to the 10 trial summary data in
Table 1 yields an estimate of 478 and 678 more lb of milk in the first lactation for moderate and
intensive programs, respectively, compared to the control group. This translates to $91 and
$121 for more income from milk in the first lactation for moderate and intensive programs,
respectively, compared to the control group. This estimated increase in income more than
offsets the greater costs of the moderate and intensive programs compared to the control group
and suggests value to moderate and intensive programs.
Labor costs of group housed, free-choice feeding programs might be lower than individually
housed, hand-fed programs. Karszes (2012) estimated costs in the first 13 weeks of age on 22
farms in NY, USA. Labor costs in group-housed programs were estimated to be $0.83/calf daily
compared to $1.36/calf daily with individually housed calves. Additionally, other non-feed and
labor costs were $1.25/calf daily in group-housed programs compared to $1.05/calf daily in
individually housed programs.
Practically on farms, there are some opportunities to improve the fat and fatty acid profile of
calf diets. Minimize or avoid addition of fat and oil to calf starters and growers will typically
lower the cost of a feed. Minimize or avoid using high fat and oil ingredients like soybeans and
distiller’s grains. These options will help to minimize the linoleic acid content of the diet that is
typically high. Supplement commercial sources of butyric acid, medium chain fatty acids, and
linolenic acid to milk or MR, starters, and grower feeds. The cost is less than $1 per bag to milk
formulas and less than $15/ton to starters and growers. This calculates to less than $1 per calf
when supplemented to the milk formula or the starter feed pre-weaning and approximately $3
per calf when supplemented post-weaning. Correcting the fatty acid concentrations of the calf
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diets in these ways reduce the costs associated with health issues, lowers the cost of body weight
gain approximately 4 to 5% when improving calf ADG approximately 7 to 10% over the first 4
months of life.
The amino acid profile of a MR is also practical to improve with little increase in feed costs. A
9% improvement in ADG pre-weaning in conventional MR programs with no change in feed
cost is an 8% reduction in feed cost per unit body weight gain. A 15% improvement in ADG
pre-weaning in moderate intensive MR programs with no change in feed cost is a 13% reduction
in feed cost per unit body weight gain. Formulating a MR for amino acid requirements versus
CP allows for a MR that is 2 to 4 percentage points lower in CP, another way to lower costs
while maintaining calf performance.
FINAL COMMENTS
Feed costs to raise calves can be substantial. Milk replacer is only a portion of the total costs to
rear a dairy calf to a milking cow but it has a high cost per lb. Understanding of how to select
the right milk replacer nutrient profile and feeding rate has been addressed with an abundance of
research over the last 10 to 15 years. Additionally, correcting for underfed nutrients (i.e.
protein, amino acids, and fatty acids) can substantially reduce feed costs per unit body weight
gain.
During cold and heat stress, conventional programs based on approximately 1 gallon of liquid
milk or MR (or 1 lb of DM) provides inadequate nutrients in many rearing and management
programs. Moderate and intensive programs have been controversial but do increase calf ADG
and possibly future milk production. When considered, they need to provide the proper protein
(amino acid) to energy ratio to achieve protein tissue and frame growth, and this type of growth
is what is possibly linked with future enhancement in milk production.
Housing cannot be overlooked. Housing that allows drafts should be evaluated in the cool and
cold weather since maintenance requirements are increased considerably in these situations.
Housing situations where the bedding does not insulate the calf (i.e. concrete, metal, wood, rock,
sand, shavings, or any type of wet bedding) increase the maintenance requirements of the calves
in cool and cold weather. During periods of hot weather, heat stress reduces calf ADG and heat
abetment systems (i.e. fans or ways to gain more airflow such as elevating the back side of poly
hutches) should be implemented.
Labor (including management) is a high cost along with many liquid diets (saleable milk or
MR) of the milk fed calf. Finding a balance between labor and feed costs is important and can
be challenging with various calf programs. Group housing, weaning age, and liquid feeding
program each impact cost and growth of calves.
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Update on Milk Fat and Human Health
A. L. Lock* and D. E. Bauman†
* Department of Animal Science, Michigan State University † Department of Animal Science, Cornell University
Corresponding author: [email protected]
SUMMARY
For over a half-century the concept of healthy eating has become synonymous with avoiding fat,
especially saturated fat and this remains a centerpiece in nutritional advice of medical societies
and government agencies worldwide. Investigations have shown the science behind this advice,
however was based on incomplete and in some cases flawed investigations. Nutritional science
has advanced rapidly and evidence now demonstrates that the proportion of total energy from fat
or saturated fat is largely unrelated to the risk of cardiovascular diseases or other chronic
diseases. Indeed there appears to be an enormous disconnect between the evidence from long-
term prospective studies and public perceptions of harm from the consumption of milk fat and
dairy products. This clearly represents a new paradigm requiring a major shift in
recommendations by national advisory groups. Furthermore, milk and dairy products are key
components in dietary patterns chosen for optimum health maintenance and the prevention of
chronic diseases.
INTRODUCTION
The importance of animal products in meeting global needs for food security is well established,
and public health organizations around the world include milk and other dairy products in
recommendations for a healthy, well-balanced diet. Dairy products are an important source for
many vital nutrients including high quality protein, energy, and many essential minerals and
vitamins (Bauman and Capper, 2011). Dairy products, however are also a major food source of
saturated fat, accounting for 20-30% of the saturated fat intake for the US population
(USDA/USDHHS, 2010). For over a half-century, saturated fat has been demonized as the
major cause of cardiovascular vascular disease (CVD) and public health recommendations are to
reduce dietary intake of saturated fat and food products containing saturated fatty acids (FA). As
a consequence, the perception of the public, and much of the scientific community, is that milk
fat is a negative component of dairy products and typical dietary advice is to consume only
reduced-fat or no-fat dairy products. The net effect of this recommendation over the last 50
years has been a progressive reduction in fluid milk consumption and a shift toward fluid milk
products containing less fat (Table 1). Recent estimates indicate that approximately 30% of our
dietary intake of saturated fat comes from dairy products with cheese being the major source
(Ervin et al., 2004).
The term CVD includes coronary heart disease, cerebrovascular disease, and other related
disorders of the heart and blood vessels. CVD is the leading cause of death in the US and
globally, accounting for about one-third of all deaths (Roger et al., 2011). Strategies to reduce
CVD involve reducing leading risk factors that include smoking, hypertension, and high
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cholesterol; doing so reduces the burden of CVD. The U.S. Center for Disease Control estimates
that about 50% of the US population has at least one of these three risk factors with CVD-
related health care costs in the US at over $400 billion annually (CDC, 2011).
New research and re-evaluation of previous research is challenging long-held dogma on the
relationship between saturated fat, milk fat, and CVD. While national organizations, health
professionals, and dietitians will be cautious in revising decade-old recommendations, there is
no doubt that the last few years have provided game-changing scientific evidence that will
revise the paradigm for the connection between saturated fat and CVD. Furthermore, these new
studies and re-evaluations have convincingly demonstrated the important role that milk and
dairy products play in health maintenance and the prevention of chronic diseases. In the
following sections we will deal briefly with some background and historical aspects related to
saturated fat and CVD, and then highlight recent findings related to the role of milk and milk fat
in human health.
Table 1. U.S. per capita availability of fluid milk. Adapted from Huth and Park (2012).
Year
Total
Consumption
Whole
milk
Reduced fat
(2%)
Low fat
(1%)
Nonfat
(<0.05%)
Liters ----------------- Percent of total fluid milk ----------------
1950 133.6 99.0 0 0 0.9
1960 125.6 95.6 0.7 0 3.1
1970 115.8 83.8 11.0 0.7 4.5
1980 99.7 62.7 24.9 7.0 5.3
1990 94.7 41.4 37.9 9.6 11.0
2000 81.4 36.5 34.2 12.5 16.2
2009 73.4 30.2 39.1 14.0 16.6
BACKGROUND AND HISTORICAL ASPECTS
Ancil Keys (University of Minnesota) played a central role in labeling dietary fat, specifically
saturated fat, as a major public health concern for CVD. Using population data obtained from
WHO reports, Keys (1953) reported a curvilinear relationship between the intake of fat and
deaths from coronary heart disease for six countries (open circles in Figure 1). Keys was
featured on the cover of TIME magazine and this was the beginning of the “diet-heart
hypothesis” proposing a sequence of etiologic relations between dietary saturated fat, circulating
cholesterol, and the development of CVD. Yerushalmy and Hilleboe (1957), however examined
the publication by Keys (1953) and concluded that many aspects were flawed including the fact
that the 6 countries had been cherry-picked from a data set for 22 countries (Figure 1). This
represented an extraordinary critique, and based on a rigorous analysis of Keys’ publication,
they concluded “The association between the percent of fat calories available for consumption
in national diets and degenerative heart disease (reported by Keys) is not valid; the association
is specific neither for dietary fat nor for heart disease mortality” (Yerushalmy and Hilleboe,
1957). Despite this, Keys (1980) continued promoting the diet-heart hypothesis and followed-up
with a seven country comparison showing that dietary intake of saturated fat as a percentage of
calories was strongly correlated with coronary death rates (r = 0.84). Again, other scientists
pointed out major flaws in his study, e.g. countries chosen by Keys to represent low saturated fat
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intake and low incidence of CVD were in fact less industrialized and differed in many ways
including smoking habits, physical activity, and obesity (Willett, 2012). Nevertheless, the diet-
heart hypothesis was well received by many health practitioners and policy makers.
Historically, serum cholesterol has served as a surrogate marker for the risk of CVD. Low-
density lipoprotein cholesterol (LDL-C) is correlated with risk of CVD; thus, the discovery that
saturated fat resulted in an increase in LDL-C provided support for the diet-heart hypothesis,
and some concluded that saturated fat must be the major cause of CVD (Ordovas, 2005). This
particularly impacted public perception of dairy products because dairy fat contains 60 to 70%
saturated FA (Table 2). Additionally, it was discovered that individual FA differ in their effects
on serum LDL-C; whereas most saturated FA were neutral, lauric acid (C12:0), myristic acid
(C14:0), and palmitic acid (C16:0) caused pronounced increases in LDL-C (Hegsted et al.,
1965) and these three FA represent about 40% of total milk fat (Table 2). This led to the
development of an atherogenic index which ranked foods based on their content of these three
FA (Ulbricht and Southgate, 1991); needless to say, the atherogenetic index ranked dairy
products as problematic with respect to CVD risk.
Figure 1. Relationship between percent of calories from fat and mortality from atherosclerotic
and degenerative heart disease. Six countries (open circles) selected by Keys (1953) from a
WHO data set for 22 countries (unselected countries shown by solid circles). Adapted from
Yerushalmy and Hilleboe (1957) and Maijala (2000). Relationship for the six selected countries
represented the foundation for Keys diet-heart hypothesis to explain cause of cardiovascular
disease.
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Public health recommendations in the 1970s and 1980s were to dramatically reduce the intake of
saturated fat. This included recommendations to reduce intake of dairy products and/or a shift to
low-fat or no-fat dairy products. One specific recommendation was to replace butter with
margarine, and this was particularly unfortunate as it markedly increased the risk of CVD for
millions of people; during this era margarine had high levels of trans FA and subsequent
research has established that intake of industrial sources of trans FA are a major risk for CVD
(Gebauer et al., 2011; Lock and Bauman, 2011). Much of the case against dairy foods is linked
to an imperfect understanding of cholesterol as a surrogate marker of CVD risk. In addition to
effects on LDL-C, saturated FA, in particular lauric acid, myristic acid, and palmitic acid cause
an increase in serum high-density lipoprotein-cholesterol (HDL-C) and this cholesterol fraction
reduces the risk of CVD. Thus, when changes in both LDL-C and HDL-C are considered,
saturated FA have no adverse effect on serum cholesterol as a risk factor for the incidence of
CVD. A meta-analysis by Mensink et al. (2003) provides convincing evidence for this; using
data from 60 clinical studies, they evaluated CVD risk on the basis of ratio of serum total
cholesterol:HDL-C. As illustrated in Figure 2, ratios for lauric acid, myristic acid, and palmitic
acid provide little or no evidence for an atherogenic effect when compared to an isoenergetic
carbohydrate substitution; in fact the ratio for lauric acid was significantly decreased. When
compared by fat type, the meta-analysis revealed no effect of saturated FA when compared to
carbohydrate substitution on an isoenergetic basis (Figure 2). Nonetheless, changes in the ratio
of serum total cholesterol:HDL-C were indicative of the well-established beneficial effects of
monosaturated and polyunsaturated FA and the increased atherogenic risk of trans FA. Thus,
this classic meta-analysis utilizing cholesterol-related surrogate markers provides no support for
saturated fat in general or the major individual saturated FA in milk fat as risk factors in CVD.
Table 2. Fatty acid composition of retail milk samples in the United States. Adapted from
O’Donnell-Megaro et al. (2011). Milk samples were obtained from 56 milk processing plants
representing all US regions and seasons over a 12-month period.
0
5
10
15
20
25
30
4:0
6:0
8:0
10:0
12:0
14:0
16:0
18:0
18:1
tran
s
18:1
cis
18:2
n-6
18:3
n-3
CLA
Oth
ers
g/1
00
g F
att
y A
cid
s
Fatty Acid
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145
For the last 50 years medical societies and government agencies have embraced the concept that
nutrition, specifically saturated fat, is a major player in the epidemic of CVD. As discussed
previously, the diet-heart hypothesis and the use of LDL-C as a surrogate marker were
perceived to offer support for this concept. Acceptance by the scientific community, however,
was far from unanimous (e.g. Ravnskov, 2002; Weinberg, 2004; Ordovas, 2005) and a growing
body of scientific studies offered no support (see discussion in Lock and Bauman, 2011). The
classic study by Mensink et al. (2003) discussed above was of special importance in challenging
the dogma on the relationship between dietary saturated fat, serum cholesterol, and incidence of
CVD. An important recent investigation was that by Siri-Tarino et al. (2010). This meta-analysis
of 21 prospective epidemiologic studies covered a 5 to 23 year follow-up of 347,747 subjects
and again results indicated “there is no significant evidence that dietary saturated fat is
associated with an increased risk of coronary heart disease or CVD” (Siri-Tarino et al., 2010).
Clearly, the relationship of fats including saturated fats, cholesterol, and CVD is more complex
than initially thought and the risk of CVD is multifaceted.
Figure 2. Meta-analysis (n = 60 trials) to examine changes in serum ratio of total cholesterol to
HDL-cholesterol when carbohydrates constituting 1% of energy are replaced isoenergetically
with fatty acids (Mensink et al., 2003). Panel A represents comparison of saturated, cis-
monounsaturated, cis-polyunsaturated, and trans-monounsaturated fatty acids (*=P<0.05;
¥=P<0.001). Panel B represents comparison of lauric acid (12:0), myristic acid (14:0), palmitic
acid (16:0), and stearic acid (18:0) (*=P<0.001). Mensink et al., 2003).
cis Polyunsaturated fatty acids
cis Monounsaturated fatty acids
trans Monounsaturated fatty acids
Saturated fatty acids
*
0.06
0.02
0.04
0.00
-0.02
-0.04
ΔT
ota
l:H
DL
Ch
ole
ste
rol
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ota
l:H
DL
Ch
ole
ste
rol
Stearic acid
Palmitic acid
Myristic acid
Lauric acid
A B
cis Polyunsaturated fatty acids
cis Monounsaturated fatty acids
trans Monounsaturated fatty acids
Saturated fatty acids
*
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cis Polyunsaturated fatty acids
cis Monounsaturated fatty acids
trans Monounsaturated fatty acids
Saturated fatty acids
cis Polyunsaturated fatty acidscis Polyunsaturated fatty acids
cis Monounsaturated fatty acidscis Monounsaturated fatty acids
trans Monounsaturated fatty acidstrans Monounsaturated fatty acids
Saturated fatty acidsSaturated fatty acids
*
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ota
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Stearic acidStearic acid
Palmitic acidPalmitic acid
Myristic acidMyristic acid
Lauric acidLauric acid
A B
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RECENT DEVELOPMENTS IN SATURATED FAT AND MILK FAT
Dietary recommendations by nationally recognized bodies have a substantial impact on the
nutrition and health community. The 2010 Dietary Guidelines for Americans recommended
restricting the consumption of saturated fat to less than 10% of total dietary calories
(USDA/USDHHS, 2010). In a peer-reviewed publication Hite et al. (2010) challenged this
report, including its specific conclusions regarding saturated fat, and pointed out that
recommendations were based on science that was inaccurately represented and summarized (as
we have discussed in the previous section), and even more serious that the report failed to
include the full body of relevant research. Hoenselaar (2012) took this a step further in a peer-
reviewed publication by examining recommendations on saturated fat from the report by
USDA/USDHHS (2010) as well as reports from two additional important US and European
advisory committees – the Institute of Medicine (IOM, 2005), and the European Food Safety
Authority (EFSA, 2010). He summarized the recommendations from these advisory committees
as follows:
1. Consume less than 10% of calories from saturated FA, replacing them with
monounsaturated and polyunsaturated FA (USDA/USDHHS, 2010).
2. Keep the intake of saturated FA as low as possible while consuming a nutritionally
adequate diet (IOM, 2005).
3. Saturated fat intake should be as low as possible (EFSA, 2010).
These advisory committees cited studies to support their recommendations, but Hoenselaar
(2012) pointed out their conclusions were not based on a valid representation of the scientific
literature. For example, the effect of saturated fat on LDL-cholesterol and its connection to an
increased CVD risk was cited in all three reports, but concurrent beneficial effects of saturated
fat to increase HDL-cholesterol thereby reducing CVD risk was systematically ignored. It is
unfortunate that due to a focus on the small rise in blood cholesterol with milk consumption, the
debate on milk fat has never achieved a reasonable balance in the evaluation of risks and
benefits. The overall conclusions by Hoenselaar (2012) were “Results and conclusions about
saturated fat in relation to CVD, from leading advisory committees, do not reflect the available
scientific literature”. Two additional public health advisory committees are the World Health
Organization (WHO) and American Heart Association (AHA). Although recommendations by
these two bodies were not included in the critiques by Hite et al. (2010) and Hoenselaar (2012),
their assessment would also apply to them. The WHO recommends saturated fat intake be
reduced to less than 10% of dietary calories and the 2009 Guidelines by AHA recommends
saturated fat be reduced to an even lower <7% of total calories (Huth and Park, 2012).
Support for a paradigm shift in conclusions for the relationship between saturated fat, milk fat,
and cardiovascular health also comes from recent reviews of the published literature. The
comprehensive reviews of Parodi (2009), Givens and Minihane (2011), Kratz et al. (2012), and
Huth and Park (2012) reached a similar conclusion – that the majority of observational studies
have failed to support an adverse association between the intake of dairy products and CVD,
regardless of milk fat levels, and in many cases a long-term beneficial effect was observed.
Several excellent investigations have been reported in the last three years and key studies are
summarized in Table 3. de Oliveira Otto et al. (2012) conducted a multi-ethic study examining
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the relationship between consumption of saturated dairy fat and CVD; they concluded that “a
higher intake of saturated fat was associated with lower CVD risk”. Importantly, the authors
found that associations between saturated fat and incident CVD depended on the food source,
with the consumption of dairy saturated fat being inversely associated with risk (risk was 0.62
when 5% of energy was from dairy saturated fat; de Oliveira Otto et al., 2012). These findings
raise the possibility that associations of foods that contain saturated fat with health may depend
on specific FA present in these foods or the complex mixture of other food constituents, in
addition to saturated fat (de Oliveira Otto et al., 2012).
Elwood et al. (2010) conducted a meta-analysis of prospective cohort studies to examine
associations between the intake of milk and dairy products and the incidence of ischemic heart
disease and stroke. Results indicated “a reduction in risk in subjects with the highest dairy
consumption relative to those with the lowest intake”; relative risk values were 0.92 for
ischemic heart disease and 0.79 for stroke (Figure 3; Elwood et al., 2010). Goldbohm et al.
(2011) reported results from a large cohort study designed to examine the association between
the intake of dairy products and mortality; data covered a 10 year period for 120,852 men and
women, and results indicated no association between dairy product consumption and stroke
mortality for men or women. Likewise, there was no association between total milk intake and
ischemic heart disease mortality in men, whereas a small positive association was observed for
women (relative risk = 1.07; Goldbohm et al., 2011). Soedamah-Muthu et al. (2011) conducted
a similar meta-analysis comparing intake of dairy products and the risk of CVD (including
coronary heart disease, stroke, and mortality); their meta-analysis gained greater analytical
power by including different dairy food categories and different ranges of intake. Results
demonstrated that “milk intake was not associated with total mortality, but may be inversely
associated with overall CVD risk”; relative risk for the later was 0.94 (Soedamah-Muthu et al.,
2011).
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Table 3. Summary of recent prospective cohort studies.
Reference Description/Objective Conclusion
de Oliveira Otto
et al. (2012)
Multi-ethnic study of saturated
dairy fat intake and incidence of
CVD; 5209 individuals for 10
yr period.
A higher intake of saturated fat
from dairy products was
associated with lower CVD
risk.
Elwood et al.
(2010)
Meta-analysis of cohort studies
of dairy intake in relation to
cardiac health.
Greater intake of milk and dairy
products reduced incidence of
ischemic heart disease and
stroke.
Goldbohm et al.
(2011)
Multivariate survival analysis
of case cohorts to examine
association between dairy
product intake and risk of
cardiac-related death. Data
collected over 10 yr (n=120,853
patients).
Dairy product intake had
neutral effects on mortality in
men, but in women dairy fat
intake was associated with
slightly increased mortality
from ischemic heart disease.
Soedamah-Muthu
et al. (2011)
Dose-response meta-analysis of
dairy consumption and
incidence of CVD and all-cause
mortality.
Milk intake was associated with
reduction in overall CVD risk,
but no relationship to total
mortality.
These findings are in broad agreement with the recently reported outcome of a remarkable 61-
year follow up of the Boyd-Orr cohort. This study involved the recruitment of 4,999 children in
England and Scotland in 1937-39 with causes of death recorded from 1948 (van der Pols et al.,
2009). Results demonstrated that a family diet in childhood, which was high in dairy products,
did not give rise to a greater risk of CVD or stroke mortality. Indeed all-cause mortality was
lowest in those with the highest dairy product and milk intake (basic hazard ratio for both, 0.69;
95% CI 0.57 to 0.84; P for trend <0.002). These findings are therefore suggestive that despite
milk fat being rich in saturated FA, milk has properties that are beneficial in reducing the risk of
CVD.
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Figure 3. The numbers of deaths in England and Wales in 2008 from various causes and the
risks for these causes in subjects with the highest milk/dairy consumption, relative to subjects
with the lowest milk/dairy consumption. Adapted from Elwood et al. (2010).
There are a limited number of studies that report disease rates in subjects who consume natural
dairy foods, and in those who consume reduced fat dairy foods. Results from such studies are
often confounded however due to the adoption of other health-related behaviors. The
appropriate question to ask is: Do fat-reduced milks and dairy foods provide any additional
advantage, or does the reduction in fat reduce the benefits of whole milk? Interestingly, a recent
study from Australia reported that full fat (but not low-fat) dairy consumption was inversely
associated with cardiovascular mortality and this effect was significant (Bonthuis et al., 2010).
Compared with participants in the lowest intake group, participants in the highest full-fat dairy
intake group had a multivariable hazard ratio of 0.33 (95% CI: 0.13–0.81; P for trend = 0.05).
Conversely, a meta-analysis of prospective cohort studies by Soedamah-Muthu et al. (2012)
suggests that low-fat dairy and milk could contribute to the prevention of hypertension, whereas
total dairy intake was not significantly associated with hypertension incidence. Therefore, a
statement by German and Dillard (2004) is appropriate: “Hypotheses [about fat-reduced milks]
are the basis of sound scientific debate; however they are not the basis of sound public health
policy”.
DAIRY PRODUCTS AND HUMAN HEALTH
Consumers are increasing aware of the connection between diet and health, and scientists are
being asked to clarify the role of specific foods in health maintenance and the prevention of
chronic diseases. Multidisciplinary studies in developing countries demonstrate that when diets
of schoolchildren had little or no animal source foods, the intake of essential micronutrients was
inadequate resulting in negative health outcomes including severe problems such as poor
growth, impaired cognitive performance, neuromuscular deficits, psychiatric disorders and even
death (Nuemann et al., 2002; Randolph et al., 2007). Continued recommendations to reduce
milk fat intake may result in inadequate intakes of key nutrients in certain population groups.
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Long-term effects of milk and dairy products on health and the prevention of chronic diseases of
the general population are also of interest, and these would best be determined in randomized
controlled trials. There have been no such trials and realistically none are likely because of the
required number of subjects and the long latency period associated with chronic diseases. The
best evidence, therefore, comes from prospective cohort studies with disease events or death as
the outcome. There have a number of prospective cohort studies that have evaluated the
association between intake of milk and dairy products and the incident of chronic diseases.
Results of meta-analysis of such studies provide convincing evidence that milk and dairy
products are associated with beneficial effects for long-term health maintenance and the
prevention of chronic diseases. The beneficial effects in reducing the risk of CVD was discussed
earlier, and additional examples of chronic diseases for which consumption of dairy products
reduces risk include: diabetes, obesity, metabolic syndrome and many types of cancer (Elwood
et al., 2008; 2010; Tremblay and Gilbert, 2009; Kliem and Givens, 2011; Grantham et al., 2012;
Korhonen, 2012; Kratz et al., 2012). Overall, the science clearly demonstrates the importance of
milk and dairy products in childhood development, health maintenance, and the prevention of
chronic diseases. Indeed, linking the benefits of milk consumption with deaths from key chronic
diseases led Elwood et al. (2008) to conclude that high milk consumers have an “overall
survival advantage”.
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Use of Probiotics in Dairy Rations During Heat Stress
L. W. Hall and R. J. Collier
Department of Animals Sciences
The University of Arizona
Corresponding author: [email protected]
SUMMARY
Heat stress reduces production in lactating dairy cows.
50% of milk yield losses come from reduced feed intake and the balance is due to
consequences of physiological changes and metabolic alterations.
The physiological changes and metabolic alterations often lead to acidosis in heat
stressed dairy cows.
Feeding probiotics to heat stressed dairy cows addresses some of the metabolic issues
which occur during heat stress.
More research is needed to understand the implications of DFMs before, during and
after heat.
INTRODUCTION
Under ideal [thermoneutral] conditions the rumen is a complex microbiome that maintains pH,
temperature and mixing in an anaerobic environment. Metabolic heat is generated within the
cow and fermentation has a major contribution to this type of heat. Fermentation occurs mainly
in the rumen and also in the hindgut. Any alteration in the rumen environment can lead to
changes in microbial populations and rumen health. Hot and humid ambient conditions can
impair the cow’s ability to dissipate heat leading to a cascade of events which alters rumen and
hindgut function.
Heat stress in dairy cows perturbs homeostasis and elicits physiological responses to reduce heat
load which can impair proper rumen function. Examples include panting which leads to salivary
bicarbonate loss and respiratory alkalosis and diversion of blood flow to the skin surface to
dissipate heat load as well as reduced rumen contraction rate (Beede and Collier, 1986).
Nutritional management of lactating dairy cows during thermal stress requires a multifaceted
approach with the overall goal to reduce metabolic heat load, minimize damaging effects from
physiological responses and maintain production. Probiotics are one of the tools available to
provide benefits to heat stressed dairy cows that may reduce production losses, maintain a
healthy gut and minimize metabolic heat.
Heat Stress
Heat stress occurs when the body temperature of a lactating dairy cow is ˃ 39.4°C. High
producing dairy cows are at a greater risk to develop heat stress because of their elevated
metabolism and high feed intake relative to maintenance requirements. Elevated respiration
rates, increased body temperature, decreased feed intake, losses in reproductive performance,
health issues and decreased milk yield are observable in hyperthermic lactating dairy cows
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(Rhoads et al., 2009). Elevated respiration rate leads to increased salivary bicarbonate loss
associated with excessive drooling and respiratory alkalosis as the animal exhales excessive
amounts of carbon dioxide. The animal responds to respiratory alkalosis by dumping increased
bicarbonate in the urine which subsequently leads to metabolic acidosis because of reduced
buffering capacity in the rumen from both salivary and urinary bicarbonate loss. Respiratory
alkalosis and metabolic acidosis occur when respiration rate increases (Sanchez et al., 1994).
Saliva is lost with panting and sodium bicarbonate is lost with excessive drooling and reduces
ruminal buffering, increasing the risk of rumen acidosis.
Feed intake drops with heat stress and milk yield also decreases. Of the decrease in milk yield,
only about 50% can be accounted for from the drop in feed intake. This was demonstrated by
pair-feeding lactating dairy cows under thermoneutral conditions the same amount of feed that
the heat stressed group consumed (Rhoads et al., 2007; Baumgard et al., 2011). There is still
50% of milk yield losses that are not directly linked with the drop in DMI. It is still uncertain
how to account for all of the losses relative to milk synthesis during hyperthermia. Nutrient
partitioning, the reduction in ruminal fermentation products (VFA and protein), and the energy
required to dissipate heat during heat stress may account for milk yield losses.
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IMPLICATIONS OF HEAT STRESS
Figure 1. Summary of production changes associated with heat stress
↓ Feed intake
- Accounts for 50% loss in milk yield
↑ Respiration rate
- ↑Expired CO2
* Renal compensation of bicarbonate (less to buffer
rumen)
- ↑Drooling
* Saliva
∙ Loss of buffers
∙ Mineral loss
∙ Water loss
↑ Rumen acidosis
- ↑ Fermentable carbohydrate to the hindgut = hindgut
acidosis
- ↓ Protozoa and fungi
- ↓ Rumination
- ↓ pH
* Protonation of NH3 to NH4
* ↑ VFA
* ↑ Streptococcus bovis = lactic acid production
(10x strength vs VFAs)
∙ Surpass limited buffering capacity
∙ Lower pH ↑ Lactobacillus
- Damage rumen wall and alters absorption
* Lactate - lowers blood pH
* Bacteria and myotic organisms invade rumen
wall - ruminitis
* Microbes pass rumen epithelium
∙ liver abscesses
- Laminitis
* Vasoactive substances
Cellular response
- HSP
- Mammary cell transport function
Post absorptive energetics
- ↑ Glucose disposal rates
- ↓ Glucose for milk synthesis
- ↑ Insulin
- ↓ Circulating NEFAs
↑Body and metabolic heat
↓Milk Yield
↑Health issues including mastitis, morbidity and mortality
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Acidosis
The excessive loss of CO2 from panting leads to respiratory alkalosis (West 2003) and the
kidneys compensate in part by excreting more bicarbonate in the urine which reduces available
buffering capacity in the rumen saliva has many important functions in ruminants, many that are
impaired by heat stress. When panting occurs salivary buffers, minerals and water are lost from
drooling. This can lead to lactic acidosis that can cause ruminitis, metabolic acidosis, laminitis,
liver abscesses and sickness (Lean et al., 2000). When rumen pH goes below 6.5, NH3 is
converted to NH4 transitioning it from a base to a weak acid. Initial increases in VFA
production with heat stress can reduce pH depending on the buffering capacity.
Rumen acidosis can occur during heat stress. In one study, the mean ruminal pH dropped from
~6.3 to 5.8 when environmental heat load was increased (from 18.3°C to 29.4°C, Mishra et al.,
1970). There is also a reduction in rumination associated with the loss of essential buffers
during heat stress. Acidosis will decrease digestion and increase undigested fermentable
carbohydrate concentrations. The availability of nonstructural carbohydrates can alter microbial
populations and increase the passage of carbohydrates to the hindgut. Streptococcus bovis, in
particular will thrive when large amounts of starch are present and produces lactic acid that is
10x stronger than VFAs (Russell and Hino, 1985). When lactic acid increases the pH drops
making the rumen environment more acidic. An increase in acidity promotes growth of some
microbes including S. bovis and Lactobacillus which will accelerate their growth rate further
decreasing the pH. Protozoa and fungi die in acidotic conditions which reduces the outflow of
nutrients from the rumen.
In addition, the increase in acidity can damage rumen wall epithelium and alter permeability.
Lactate can be absorbed across the rumen wall and lower the pH of blood. Bacteria can invade
the rumen epithelium and cause ruminitis or make it to the liver where organisms such as
Fusobacterium necrophorum and Archanobacterium sppcan cause abscesses (Bolton and Pass,
1988). The liver is vital to gluconeogenesis and performance can be impaired after the
occurrence of heat stress.
When the rumen becomes too acidic the composition of rumen microbiota can change. Coupled
with the increased permeability of the rumen, vasoactive substances can alter blood flow and
can increase laminitis. These substances include lactate, serotonins, histamine and endotoxins
(Westwood and Lean, 2001) and can be absorbed through the compromised rumen and large
intestine. Endotoxin release results from acidosis killing gram-negative bacteria in the rumen
and the large intestine (Dong et al., 2011). Grain induced ruminal acidosis has been shown to
increase gram-negative Escherichia coli, a potential source of the endotoxin lipopolysaccharide
(LPS) (Khafipour et al., 2009). Endotoxin can generate a nonspecific immune retort called an
acute phase response (Ametaj et al., 2010). Infusion of (LPS) in lactating dairy cows decreased
DMI and milk yield and resulted in greater numbers of cows with metabolic disorders such as
displaced abomasum compared to control cows (Zebeli et al., 2011).
Hindgut Acidosis
The hindgut fermentation provides 5-10% dietary energy under normal conditions. Decreased
rumination and digestion associated with rumen acidosis can increase the passage of
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fermentable carbohydrates. When excessive fermentable carbohydrates make it the hindgut and
are fermented, hindgut acidosis can occur (Gressley, 2011). Loose stool that is foamy with
mucous indicates hindgut acidosis and possibly the sloughing of intestinal lining.
Environmental stress often causes hindgut acidosis in lactating dairy cows.
Heat Shock
Heat stress can damage proteins within a cell by causing them to unfold (denature). The up-
regulation of the cytoprotective heat shock proteins (HSP) also called chaperones during heat
stress is essential to cell survival because HSP’s repair proteins required for normal cellular
function by refolding them (Sharma et al., 2009). The cytoskeleton and transport function within
epithelial mammary cells is also impaired (Collier et al., 2008). Even though the HSPs benefit
the cell there is a nominal cost to repair misfolded proteins. Sharma et al. (2010) under in vitro
conditions determined that it cost about 5 ATPs for HSP 70 to repair one protein. However,
large scale production of heat shock proteins within mammary cells during heat stress likely
contributes to the decline in protein concentration of milk observed during warm summer
months. The protein synthetic factory of the mammary cell is diverted to increased synthesis of
protective HSP’s leading to reduced production of milk caseins.
Metabolism
During heat stress, cellular and whole body metabolism shifts. Glucose becomes a key fuel
source that heat stressed cows rely on to remain euthermic and milk synthesis becomes less
important (Rhoads et al., 2011). Heat stressed dairy cows have a greater glucose disposal rate
and the amount of glucose dedicated to milk synthesis is about 400g glucose/day less in heat
stressed cows compared to their pair-fed cohorts (Baumgard et al., 2011). Plasma insulin levels
increase with heat stress and adipose tissue is not mobilized even though the cow is in a
negative energy balance. Currently, research indicates that supplying additional glucose alone is
not sufficient to prevent these metabolic changes and does not improve milk yield in heat
stressed lactating dairy cows.
PROBIOTICS
The use of probiotics in lactating dairy cows is a widely accepted method to maintain a healthy
rumen. Direct fed microbials (DFM) include active cultures or vegetative forms of bacteria and
yeast. DFMs can improve anaerobiosis, maintain pH, and improve feed efficiency. The rumen
microbiota is responsible for the majority of energy requirements. Rumen fermentation supplies
gluconeogenic precursors, microbial proteins, and other gasses such as methane.
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Figure 2. Saccharomyces cerevisiae strain CNCM I-1077 (Levucell SC2, Lallemand, Toulouse,
France) and the changes in pH at thermoneutral conditions. Adapted from Bach et al., (2007).
The effectiveness of a probiotic may depend on the flora from individual cows or dairies.
Changes of host microbial populations to environmental/ nutritional stimuli can be host specific.
A study out of Lethbridge, AB, Canida looked at changes in ruminal variables in Holstein
heifers in their first lactation fed a high concentrate or high forage diet. Each animal was
classified as least, intermediate and most acidotic. Variables included changes in pH and
bacterial community compositions (BCC). Production responses were similar between groups
and not effected by rumen acidosis. Differences in BCC were seen in individuals and not
specific to treatment or classification (Mohammed et al., 2012).
Enhancing production can be accomplished through different methods and strains of probiotics.
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Figure 3. Targets of DMFs not specific to heat stress
Maintain pH in HS rumen and improve feed efficiency
–Levucell® SC (Lallemand)
•Yeast, strain S. cerevisiae I-1077
Lactic acid-utilizing microbes
–Lactipro® (MS Biotec)
•Bacteria, strain Megasphaera elsdenii NCIMB
41125
Favorable VFA profile
Stimulating activity of beneficial rumen bacteria
–Yea-Sacc® (Alltech)
•Yeast, Saccharomyces cerevisiae CBS 493.94
Maintain healthy microbes
–Calsporin® (Calpis)
•Bacterial spore, Bacillus subtilis C-3102
Improve Immune response to
–OmniGen-AF
•Yeast + B-complex vitamins
Additionally, each product has other claims and was placed in grouping by research, observation
or claims. If DFMs can reduce acidosis, promote beneficial microbial flora or elicit a favorable
immune response, the impact, severity and duration of hyperthermia may be reduced.
Benefits have been documented when DFMs were fed to HS dairy cows. Shwartz et al., (2009)
fed two strains of yeast with endogenous enzymes to HS lactating dairy cows. Though there
were no production differences, treatment reduced rectal temperature at 1200 and 1800 h. To
address the challenges of heat stress, the approach will likely address different aspects of heat
stress.
Betaine is an organic osmolyte that has been shown to promote favorable bacterial growth under
stressed condition (Wdowiak-Wrobel et al., 2013) including fluctuations in pH (Laloknam et al.,
2006). Yeast extract that contain oligosaccharide can act as a prebiotic and promote favorable
microbial growth. Future research with cocktails/ combinations of probiotics and other
promoters may answer broader basic and applied questions. Celmanax® contains hydrolyzed
yeast, yeast extracts and yeast culture and has a claim to improve milk production and reduce
somatic cell count. Research supports the finings that yeast cultures can influence microbial
metabolism (Miller-Webster et al., 2002) and can stimulate lactic acid utilizing bacteria (Nisbet
and Martin, 1991).
Lactating dairy cows were fed 4 x 109 cfu/ head of Lactobacillus acidophilus NP51 and
Propionibacterium freudenreichii NP24 for 12 weeks between June and September. No
differences were found respiration rates or body temperature. Feeding the DFM increased milk
yield by 2.4 kg/day, improved protein yield and improved digestibility (Boyd et al., 2011).
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Huber et al. (1994) reported that the addition of fungal culture increased milk yield and cellulose
digestibility in some studies. The fungal cultures also decreased body temperature and
respiration rates in hot weather, but not in cool.
The use of probiotic Lactobacillus GG (ATCC strain number 53103) in young adult mice colon
(YAMC) cells induced heat shock expression. Expression was induced in thermoneutral and
heat stress (Tao et al., 2006). Current research at the University of Arizona is measuring the
expression of HSP70 and HSP27 in DFM treated lactating cows subjected to heat stressed
conditions (R.J Collier lab).
Preconditioning animals for heat stress needs to be further studied. DMFs can be fed during
non-stressed conditions to prevent the amplification of metabolic disturbances during heat
stress. Many of the unknowns (Table 1) do not have sufficient data. Some of the responses to
probiotic and heat stress (Table 1) need additional research for replication, strain and
combination therapy during heat stress
Table 1. Observed responses to heat stress and/ or Probiotic
Observed Responses
Item Heat stress (HS) Probiotic (non HS) Probiotic1 HS
Feed intake Reduced ↓ Increased↑
Improved
Feed efficiency Reduced ↓ Increased↑
Increased↑
Respiration rate Increased↑ n/a
Reduced ↓
Drooling Increased↑ No change
Unknown
Rumen acidosis Increased↑ Reduced ↓ Reduced ↓
Hindgut acidosis Increased↑ Reduced ↓ Unknown
Microbe community Altered2
Improved
Unknown
Body temperature Increased↑ Unknown
Reduced ↓
Milk yield Reduced ↓ Increased↑
Increased↑
Morbidity Increased↑ Reduced ↓ Unknown
HSP Increased↑ Increased↑
Increased↑
CONCLUSION
Some of the metabolic alterations that occur with the insult of heat stress can be addressed
using DFMs. Preconditioning cows with DFMs should be examined to measure the effect during
and while recovering from heat stress. Replacement dairy heifers may be the extreme example
with opportunities to influence both hindgut and rumen microbial populations (Dick et al.,
2012). Neonatal calves are functional monogastrics and subject to scours. Later as the rumen
develops DFM supplementation can promote favorable microbial growth DMFs have the
potential to alter fore and hindgut microbes to improve growth, development and improve future
lactations. If a DFM is fed to a postnatal calf it can potentially influence the microbial flora in
the large intestine prior to rumen development. As the rumen matures in the first few months of
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a calf’s life, the addition of DFMs may promote a healthy rumen and improve the rumen wall
development.
Reducing acidosis during HS can minimize production losses and prevent metabolic and health
disorders. DMFs offer lactic acid utilizing and promoting microbes and more favorable VFA
and nutrient production. Supplying heat stressed cows with improved gluconeogenic precursors
can allow the animal to dissipate heat and acclimate to heat stress.
Comparisons can be inconsistent due to individual and herd variability and the type of probiotic
used. Some commercial products include prebiotics, vitamins, minerals and other growth
promoters. DFM feed additives are a promising approach to reducing the impacts of heat stress.
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ARPAS
The American Registry of Professional Animal Scientists
(www.arpas.org)
Southwest Nutrition & Management Conference
February 21 & 22, 2013
Approved for up to 10 CEU’s:
Pre-Conference Symposium – 2 CEU’s
Thursday Conference Sessions – 4 CEU’s
Friday Conference Sessions – 4 CEU’s
As a registrant of the SWNMC (if you are an ARPAS member) you may include these credits
on your annual submission of CEU’s in the fall. A CEU reporting form will be included with
your dues notice OR you may download a form from their website. Your CEU’s can be most
efficiently recorded by sending in one form at the time you submit your membership renewal in
the fall.
ARPAS Business Office
1111 N. Dunlap Ave.
Savoy, IL 61874