There has been tremendous interest in understanding the biology of the dairy cow transitioning from late pregnancy into lactation. This interest is evidenced by documentation that most dairy cow disease issues occur within the first few weeks of lactation.
Intensive research over the past decades has addressed clinical hypocalcemia, better known as milk fever, and recognized subclinical hypocalcemia (now termed dyscalcemia) as critical “gateway diseases” increasing the risk of other postpartum disease events.
Although the use of dietary cation-anion difference (DCAD) concept in feeding the late pregnant cow is strongly supported by research in preventing both forms of hypocalcemia, its adoption by dairy farms is approximately 27% based on the National Animal Health Monitoring System (NAHMS) across reports from 2002 to 2014. In the NAHMS (2014) report, large farms (greater than 500 cows) utilize this technology to a greater extent (54.5% of operations). In this same report, 68.9% and 43.8% of all dairy operations administer calcium, as an injection, drench or bolus, and propylene glycol, as a drench or feed supplement, respectively. This would suggest there remain transition cow health issues costing the producer in milk loss, animal loss and disease treatment costs, reducing overall farm productivity and profitability.
What makes it so challenging to define appropriate feeding and management practices of transition dairy cows to achieve reasonable disease prevention strategies? Part of the problem is the tremendous variability in farm systems, management and feeding practices.
Fundamentally, we still have not defined a key issue or issues that lead to postpartum disease risks. In the 1990s, much research focused on the decline in dry matter intake that occurs as the pregnant cow approaches calving and its association with negative energy balance, leading to increased blood concentration of nonesterified fatty acids (NEFA). The reason why this is important is the high association of blood NEFA concentration prior to and immediately following calving and the increased risk of postpartum disease events. Negative energy balance or NEFA concentration alone do not account for transition cow disease risk, as some highly productive cows can maintain health in the face of high blood NEFA concentrations.
The duration and severity of the decline in prepartum intake just prior to calving has been associated with greater risk for various disease conditions postpartum. If the consequence of lower dry matter intake, higher NEFA concentration, is not the key factor, what is causing the decline in intake? This is where systemic inflammation may play a role and consequently change our paradigm of understanding transition cow disease risk.
Inflammation is a term often used, similar to stress, without a complete understanding of what it is and does. Inflammation is a physiologic response of specific cells to some insult, such as trauma or disease, initiating the immune system to defend the body.
Immune surveillance cells, namely macrophages, are found in all tissues of the body and are the first to recognize a problem. The cells become activated and release pro-inflammatory mediators locally in the tissue to stimulate changes in cells lining the blood vessels to start the inflammatory process.
In response to these pro-inflammatory mediators, blood flow in the affected region increases and blood vessels become “leaky,” allowing more fluid, proteins and immune cells to move from blood vessels into the tissue. The stimulated blood vessel cells then release other mediators such as prostaglandins to further support the inflammatory response. Collectively, these responses are responsible for the cardinal signs of inflammation: swelling, pain, redness, heat and loss or altered function.
The goal of inflammation is to destroy the pathogen or trauma damage and regenerate normal functional tissue at the insult. As described, the inflammatory response is a very beneficial component of the immune response, protecting the animal from disease. As with many biologic functions, however, chronic or excessive inflammatory response can be detrimental.
These pro-inflammatory mediators not only have effects locally at the site of trauma or infection but also travel systemically to stimulate the liver to produce various acute phase proteins to help in this process. System pro-inflammatory mediators also can influence body-wide physiologic responses, most notably, increased body temperature (i.e., fever), breakdown of body fat and protein, and increased glucose utilization.
Pro-inflammatory mediators have a profound effect to suppress appetite in the face of increasing rate of metabolism. Recent work from Iowa State University showed cows stimulated with a pro-inflammatory agent metabolically consumed large quantities of glucose to support the activated inflammatory and immune response, as all immune cells are obligatory consumers. This situation would divert available blood glucose to support inflammation rather than milk production, thus accounting for lower milk production in diseased cows.
So what does this all mean relative to the transition cow and disease risk? As discussed, a greater decline in dry matter intake prior to calving seems to be a factor in creating a greater risk for a cow having a postpartum disease. We know that the decline in intake is not due to cows expecting to become sick. What is being considered are environmental stressors such as heat stress, overcrowding of transition pens, social upheaval of pens, as well as cow factors such as somatic cell count and milk production at dry off and rapid increases in dietary starch leading to “leaky gut.” All potentially induce an inflammatory response.
Depending upon the severity and multiplicity of insults, the pro-inflammatory response could induce a higher magnitude or prolonged decline in dry matter intake, starting a period of negative energy and protein balance. Calving induces a profound inflammatory response, which is heightened with any dystocia or abnormal birthing. The filling of the mammary gland with colostrum, then milk, will also increase inflammation with exposure to potential mastitis pathogens. Postpartum inflammation can continue to negatively impact dry matter intake, further increasing negative energy and protein balance. In this nutritionally depleted state, cows will be more susceptible to metabolic and infectious diseases and have impaired reproductive performance.
This perspective seems quite reasonable in addressing our transition cow challenge. Do we want to eliminate the inflammatory response? The answer is no. We do need some inflammation response to address tissue trauma at calving, removal of fetal membranes and mastitis disease risk with lactation. However, we do not want the inflammatory response to be ongoing and excessive.
In another article, a targeted approach to treating only high-risk cows and heifers is described, aiming to minimize the excessive inflammatory response that has detrimental effects and maintain a more physiological inflammatory response in low-risk cows. For our transition management, we need to be cognizant of potential stressors in our system to minimize an overstimulation of the inflammatory response. Minimize major changes in the diet that might lead to foregut or hindgut acidosis and initiate a leaky gut condition that allows more inflammation-stimulating substances to be absorbed.
Management of inflammation may not be the only answer to transition cow health issues, but it does provide a more unifying understanding of how environmental, nutritional and management issues may contribute to the success or failure of the transition cow.
