A D V I S O R Y
h e a lt h y h e r d m a n a g e m e n t r e p o r t
D.L. O’Connor
Dairy Technology Manager
Prince Agri Products, Inc.
Heat Stress and Immunity in Dairy Cows
Introduction
The effects of heat stress are estimated to cost the dairy industry
$897 million annually (St. Pierre et al., 2003). Primary losses
are associated with, but not limited to, lowered milk production,
increased metabolic disorders, poor reproduction and reduced
immune function (Wheelock et al., 2010).
Temperature Humidity Index (THI)
Heat stress in the dairy cow has been defined as the point at
which rectal temperature exceeds 39.2°C (102.6°F) with breaths
exceeding 60/minute.
Temperature Humidity Index (THI) is calculated based on the
relationship between environmental temperature and relative
humidity. Lactating dairy cows experience heat stress when THI
rises above 72, with severe heat stress occurring when THI
exceeds 88 (Thatcher et al., 2010).
The table below (Table 1) illustrates various temperatures and
humidity values that yield a THI of 72, the point at which signs of heat
stress begin to develop in the dairy cow. For example, a temperature
of 80° F, with a relative low humidity value of 35%, will yield a THI of 72
and create conditions that could impact the health and performance
of a dairy cow.
Factors such as level of milk production, air movement, sun exposure
and duration of these conditions may impact THI values, such
that animals may experience more severe heat stress at lower
temperature and relative humidity values (Thatcher et al., 2010).
Table 1: Temperature and Humidity
combinations yielding a THI of 72 (Zwald, A., 2007)
Temperature °F
Relative Humidity %
72
100
74
80
76
60
80
35
84
15
Higher producing dairy cows show more profound symptoms of heat
stress as they generate more heat while eating more feed to support
higher production levels.
Most dairymen, veterinarians and dairy nutritionists understand
the impact that heat stress can have on milk production and dry
matter intake, the most common symptoms for cows experiencing
moderate heat stress (Table 2).
Table 2: Relative changes in expected dry matter intake
(DMI) and milk yield and water intake with increasing
environmental temperature
Expected Intakes and Milk Yields
Temperature °F
DMI (lbs.)
68
40.1
59.5
18.0
77
39.0
55.1
19.5
86
37.3
50.7
20.9
95
36.8
39.7
31.7
104
22.5
26.5
28.0
Milk Yield (lbs.) Water Intake (gal)
Sources: National Research Council. 1981. Effect of
Environment on Nutrient Requirements of Domestic
Animals. National Academy Press, Washington, D.C. Dr. Joe
West, Extension Dairy Specialist, University of Georgia.
Heat Stress and Immune Dysfunction
With the development of gene expression microarrays, dairy
scientists are now able to study the impact that heat stress has
at the cellular level. It has long been established that stress
in the dairy cow activates the hypothalamic - pituitary - adrenal
axis. Activation of this gland causes an increase in plasma
glucocorticoids (cortisol) (Figure 1).
Figure 1: Impact of stress on glucocorticoid release
(Burton, 2007)
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Heat Stress and Immunity in Dairy Cows
Acute exposure to high environmental temperatures has
been shown to cause significant increases in plasma cortisol
in dairy cows (Stott et al., 1970). It is also well documented
that increases in circulating plasma cortisol result in downregulation or suppression of L-selectin expression on the
surface of neutrophils (Figure 2).
Neutrophils harvested from dairy cows exposed to heat stress
during the dry period and at the time of calving demonstrated
reduced oxidative burst and phagocytic activity at 20 days postcalving compared to cows that had been cooled, indicating
a carryover effect of heat stress on immune function into
lactation (do Amaral et al., 2011).
Figure 2: Relationship between cortisol and neutrophil
L-selectin, a marker of immune function (Burton and Erskine, 2003)
3.5
Cortisol
4.0
Neutrophil L-selectin
3.0
Cortisol (ug/dl)
3.5
2.5
3.0
2.5
2.0
2.0
1.5
1.5
1.0
1.0
Neutrophil L-selectin
4.5
0.5
0.5
0
0
-8
-4
0
0.25
0.5
1
1.5
2
7
Days Relative to Parturition
Neutrophils are considered to be the first line of defense
against invading pathogens and L-selectin is a marker of
innate immunity in dairy cows (Weber et al., 2004). Reduced
L-selectin expression causes neutrophils to function poorly by
failing to move into tissue being invaded by pathogens. This has
a dramatic negative impact on the immediate response of the
immune system to disease challenges and the clinical outcome
following exposure to an infective organism (Kansas, 1996).
Transition Cow Immunity
Additionally, increases in circulating cortisol as a response
to heat stress cause an increase in cellular levels of other
markers of immunity known as heat shock proteins (HSP)
(Collier et. al., 2008). Heat shock proteins (HSP) function to
fortify and protect cells during a stressful event and have been
shown to increase at the onset of hyperthermia.
This can occur not only at the time of calving but at other
times throughout the lactation cycle when dairy cows may be
exposed to other types of stress, such as heat stress, which also
compromises animal immunity.
Cows with compromised immune systems are predisposed to
mastitis and other types of infectious and metabolic diseases
(Goff and Kimura, 2002).
Heat shock proteins function as a danger signal to the immune
system to encourage increased killing of pathogenic bacteria
by neutrophils and macrophages, innate immune cells and the
first line of defense against invading bacteria (Campisi et al.,
2003; do Amaral et al., 2011).
Neutrophils work to kill and contain invasive pathogens through
processes known as phagocytosis and oxidative burst activities.
These killing activities have been shown to be depressed in
response to changes in circulating cortisol levels associated
with stressful events (Heasman et al., 2003; Burton et al.,
2005).
The transition period is one of the most challenging times for
the dairy cows’ immune system. Reduced immune function
associated with failure of neutrophils to move into tissues being
invaded by pathogens and reduced capability of neutrophils and
other immune cells to effectively carry out phagocytosis and
killing mechanisms for pathogens allow the dairy cow to be highly
sensitive to infectious disease.
Management strategies to improve neutrophil function during
times of stress will likely improve immune function and aid in
disease resistance. “Prepping” of the dairy cows’ immune
system to mobilize large numbers of neutrophils into circulation
may provide a defensive edge against infectious organisms, such
as those associated with mastitis (Burton and Erskine, 2003).
A D V I S O R Y
References
Burton, J.L. and Ronald J. Erskine. 2003. Immunity and mastitis: Some new ideas for an old disease. Vet Clin Food Anim 19:1–45.
Burton, J.L. 2007. Stress, Immunity, and Mammary Health. Presentation at California Animal Nutrition Conference Pre-Conference Technical Symposium;
Fresno, CA.
Campisi, J., T.H. Leem, and M. Fleshner. 2003. Stress-induced extracellular Hsp-72 is a functionally significant danger signal to the immune system.
Cell Stress Chaperones 8:272–286.
Collier, R.J., J.L. Collier, R.P. Rhoads, and L.H. Baumgard. 2008. Invited Review: Genes Involved in the Bovine Heat Stress Response. J. Dairy Sci. 91:445–454.
do Amaral, B.C. , E.E. Connor, S. Tao , M.J. Hayen, J.W. Bubolz, and G.E. Dahl. 2011. Heat stress abatement during the dry period influences metabolic gene
expression and improves immune status in the transition period of dairy cows. J. Dairy Sci. 94:86–96.
Goff, J. and K. Kimura. 2002. Factors Affecting the Health and Disease Resistance of The Transition Cow. PSU Dairy Cattle Nutrition Workshop. Grantville, PA.
Heasman, S.J., K.M. Giles, C. Ward, A.G. Rossi, C. Haslett and I. Dransfield. 2003. Glucocorticoid-mediated regulation of granulocyte apoptosis and
macrophage phagocytosis of apoptotic cells: implications for the resolution of inflammation. Journal of Endocrinology 178, 29–36.
Kansas, G.S. 1996. Selectins and their ligands: current concepts and controversies. Blood 88: 3259–3287.
St-Pierre, N.R., B. Cobanov, and G. Schnitkey. 2003. Economic losses from heat stress by US livestock industries. J. Dairy Sci. 86 (E Suppl.):E52–E77.
Stott, G.H. and J.R. Robinson. 1970. Plasma corticosteroids as indicators of gonadotropin secretion and fertility in stressed bovine. Presented at: Sixty-Fifth
Annual Meeting, Amer. Dairy Sci. Ass., Gainesville, Florida.
Thatcher, W.W., I. Flamenbaum, J. Block and T.R. Bilby. 2010. Interrelationships of heat stress and reproduction in lactating dairy cows. High Plains Dairy
Conference, Amarillo, TX.
Weber, P., T. Toelboell, L. Chang, J. Tirrell, P.M. Saama, G.W. Smith, and J.L. Burton. 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. Journal of Leukocyte Biology Volume
75:815-827.
Wheelock, J.B., R.P. Rhoads, M.J. VanBaale, S.R. Sanders, and L.H. Baumgard. 2010. Effects of heat stress on energetic metabolism in lactating Holstein
cows. J. Dairy Sci. 93:644–655.
Zwald, A., 2007. Heifer Management Blueprints. Department of Dairy Science, University of Wisconsin.
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