Management Practices to Minimize Stress Factors for Transition Cows

You may be asking what this ancient riddle ("Which came first, the chicken or the egg?") has to do with dairy cows. Relative to dairy cows this riddle may be modified to ask: "Which came first, inflammation or disease?" A recent review paper published in the Journal of Dairy Science (Horst et al., JDS 104:8380, 2021) has brought into question our understanding of postpartum disease issues in the dairy cow. Postpartum diseases are the scourge of dairy production leading to significant productive, reproductive, and economic losses. Economic loss from decreased milk production is only the tip of the proverbial iceberg in evaluating total disease losses. Total financial losses associated with periparturient diseases result from lost and discarded milk, veterinary fees, increased labor, pharmaceuticals, and premature culling. Subsequent cow reproductive performance is also adversely affected by periparturient disease. Surveys have suggested that more than 50% of dairy cows calving experience one or more disease events in the period from calving through six weeks into lactation indicating a great potential area for herd improvement. In these surveys the range of disease events was highly variable between farms and should be a metric producers should evaluate as part of their transition cow management assessment.

The transition period, defined as the three to four weeks prior and following calving, has been researched extensively over the past thirty years. Even with the great strides forward with research on nutrition and management of the transition cow, we have not greatly solved problems of periparturient disease. One consistent frustration with managing transition cows is the seemingly lack of consistency in response to a given program.

Most research addressing postpartum disease has focused on excessive release of body fat in the form of non-esterified fatty acids (NEFA) and subsequent excessive production of ketone bodies (i.e., beta-hydroxybutyrate, BHB) leading to ketosis, fatty liver, displaced abomasum, and immune suppression. Immune suppression is further accentuated with hypocalcemia (i.e., milk fever) and increases the risk for retained fetal membranes, mastitis, and metritis. The release of NEFA has been related to negative energy balance due to inadequate energy intake relative to energy loss in colostrum and milk. Any factor that accentuates impaired dry matter intake will accentuate this discrepancy leading to greater fat mobilization. We understand that body condition will affect intake where over-conditioned cows have reduced intake and resultant greater body condition score loss after calving. Excessive body condition loss is known to adversely affect pending reproductive performance.

Practical applications from these research findings have focused on controlling energy intake prepartum to minimize the negative impacts of body condition excess to reduce NEFA release and minimize production of BHB. Additionally, much effort has been placed on minimizing the prevalence of hypocalcemia, either clinical or subclinical, through dietary manipulations of prepartum calcium content or cation-anion difference (DCAD) to support calcium homeostasis. In-spite-of some reduction in hypocalcemia prevalence, the industry has not made a significant dent in reducing transition cow health events.

How has this review turned our perspective of transition cow health upside down? Essentially the authors suggest we are looking at the underlying cause of transition cow problems from the wrong direction. These authors make the point that mobilization of body fat during periods of negative energy balance and production of ketone bodies are normal metabolic adaptations essential for supporting lactation. They provide some intriguing examples of whales, seals, and other species that essentially do not consume any diet during lactation and lose more than 30% of their body weight. Just think what having cows that do not require consuming feed in order to make milk could do for dairy's bottom line! Unfortunately, the authors do not comment on the difference in milk composition with these species compared to cows. Milk from seals and whales is more than 50% fat, only 12% protein, and 0.7% lactose, which is very different from cows and explains the difference in glucose needs to support milk production.

Essentially the focus of this proposed paradigm shift is accounting for activation of the immune response following disease thus causing the normal metabolic adaptions to lactation to become challenged and perturbed. The underlying issue here is maintaining glucose availability to support milk production as well as providing energy to the activated immune response. The authors provide strong evidence of the metabolic cost to maintain an active immune response, and this will alter and exaggerate the metabolic adaptations leading to elevated NEFA, ketones, and calcium homeostasis. This is not a new concept as Bertoni and colleagues published data showing cows experiencing greater inflammatory conditions were at greater risk for postpartum disease conditions and impaired reproduction (Bertoni et al., 2008). What is not really explained is how cows that go on to experience a disease event have reduced dry matter intake prepartum compared to cows with no health events postpartum (Huzzey et al., 2007; Goldhawk et al., 2009). These authors provide evidence to support activation of the immune response inhibits dry matter intake; much more than elevated blood concentrations of NEFA or BHB. So, what is causing the immune activation prior to disease occurrence?

At this point the answer to this question remains unknown. However, it is well-recognized that heat stress, overcrowding, social hierarchy disturbances, among other factors can stimulate an inflammatory response. Additionally, inflammation associated with the gut could result from dietary changes, subacute acidosis, mycotoxin presence, or feed deprivation. Although it seems the underlying premise of transition cow disease and impaired performance has been upended, the focus remains on management practices minimizing "stress" factors that might impede dry matter intake leading to disease events that will exacerbate the cow's metabolic adaptations, including a necessary immune activation transitioning from pregnancy into lactation. For more information or questions, contact Dr. Van Saun at 814-867-2038 or by email at rjv10@psu.edu.

Sources

Horst, E.A., S.K. Kvidera, L.H. Baumgard. 2021. The influence of immune activation on transition cow health and performance-A critical evaluation of traditional dogmas. Journal of Dairy Science 104:8380-8410. doi.org/10.3168/jds.2021-20330

Bertoni, G., E. Trevisi, X. Han, M. Bionaz. 2008. Effects of inflammatory conditions on liver activity in puerperium period and consequences for performance in dairy cows. Journal of Dairy Science 91:3300-3310. doi.org/10.3168/jds.2008-0995

Huzzey, J.M., D.M. Veira, D.M. Weary, and M.A.G. von Keyserlingk. 2007. Prepartum behavior and dry matter intake identify dairy cows at risk for metritis. Journal of Dairy Science 90:3220-3233. doi.org/10.3168/jds.2006-807

Goldhawk, C., N. Chapinal, D.M. Veira, D.M. Weary, and M.A.G. von Keyserlingk. 2009. Prepartum feeding behavior is an early indicator of subclinical ketosis. Journal of Dairy Science 92:4971-4977. doi.org/10.3168/jds.2009-2242