Metabolic diseases are those associated with the chemical processes necessary for maintenance of life. In cattle, metabolic diseases include errors in electrolyte/mineral metabolism, of which parturient hypocalcemia (milk fever) is most common, or errors associated with energy metabolism, including ketosis and displaced abomasum. Metabolic diseases are associated in that the occurrence of one increases the risk of another. These associations tend to leverage the impact of disease on the animal.
Parturient hypocalcemia and ketosis can be present in either clinical or subclinical states. Clinical disease implies cows exhibit physical abnormalities. Subclinical disease is one where cows do not exhibit clinical signs, but the biochemical condition is present. Most producers have been content to estimate the impact of metabolic disease as a function of occurrence of clinical disease. While clinical disease occurs at a modest rate, subclinical disease has become recognized as common.
Occurrence of metabolic disease
Clinical parturient hypocalcemia affects an average of 6 percent of cows and has been associated with a three-fold increased risk of dystocia, retained placenta and displaced abomasum and a nearly nine-fold increased risk for clinical ketosis and mastitis. Subclinical hypocalcemia has been preliminarily reported to occur in 25.3, 43.9 and 57.8 percent of lactation 1, 2 and 3+ cows, respectively.
Clinical ketosis is estimated to affect about 6 percent of cows. However, subclinical ketosis affected 59 percent of cows. Ketosis is associated with a decrease in milk production and increased risk of other postpartum diseases. It is known the risk of displaced abomasum is increased as a consequence of subclinical ketosis in lactation or in the two weeks leading up to calving.
These data may be interpreted several ways. They do suggest there are a high proportion of cows very near “the edge” of clinical disease. This further suggests any limited stressor, acting to tip the balance in favor of disease, may cause a very considerable proportion of cows to be clinically affected.
In the most parsimonious terms, metabolic disease, both electrolyte-related and energy-related, may be considered a problem associated with diet formulation, diet consumption or individual (i.e., genetic) factors. Of these, diet consumption is probably the most variable. Therefore, if a single risk factor “root cause” of metabolic disease is to be considered, that “root cause” would focus on the factors associated with dry matter intake (DMI) in late gestation or early lactation cows. This is particularly and directly the case for the energy-related diseases.
Ketosis, fatty liver disease and displaced abomasum are the common energy-related metabolic diseases. Energy-related disease is generally thought to occur as a result of excessive lipolysis (fat breakdown) that leads to ketosis or fatty liver. Lipolysis is stimulated when energy output exceeds intake. Endocrine drivers of lipolysis include decreased insulin (low insulin allows lipolysis to continue), increased glucagon (which increases lipolysis), increased glucocorticosteroids (cortisol, which increases lipolysis) and catecholamines (epinephrine/norepinephrine, the so-called “fight or flight” hormones that are powerful lipolytics).
While some of these mediators are beyond direct control, the glucocorticosteriods and catecholamines are important mediators that are, to at least a partial degree, dictated by and within control of management.
Energy-related disease occurs as a consequence of energy distress. Energy distress can be pictured as a non-adaptive or inappropriate cow response to negative energy balance. Since all cows are expected to go through a period of acute negative energy balance postpartum, the key to health is really how the cow responds to the total environmental stress. Negative energy balance occurs prior to calving, and lipid mobilization prepartum is extremely rapid. Therefore, energy distress is initiated before calving.
Classically, much focus has been placed on improving energy intake of cows through activities aimed at increasing voluntary DMI. The importance of maximizing dry period DMI has been recently questioned, and there has been some thought that stabilizing dry period DMI may be of principle concern. Irregardless of whether maximizing or stabilizing DMI is found to be of primary importance, factors that contribute to acutely decreased DMI must still be identified and controlled.
Risk factors for altered DMI
Body condition, social interaction and concurrent disease are a few of the many factors affecting DMI. It is well known that overconditioned cows (body condition score [BCS] 4.0) have a greater decline in DMI around calving, putting them in a position of susceptibility to energy-related disease. It has been suggested that adipose cells of overconditioned cows are more sensitive to signals to initiate fat breakdown, and fat cows may exhibit insulin resistance. Overconditioned cows tend to have increased fat breakdown, increased liver lipid concentration and a shift toward ketogenesis.
It appears cows near calving with BCS 4.0 have a marked propensity toward lipid mobilization, and cows with BCS 3.0 have little propensity to mobilize fat. Therefore, the recommendation that late dry cows be in a BCS range of 3.25 to 3.75 probably represents a good trade-off between subsequent milk production and risk of metabolic disease. However, careful managers may be able to maintain health and gain high production in cows with greater BCS if environmental conditions are optimal and energy distress is avoided.
Social (or grouping) stress can result in alterations of cow behavior and may affect energy balance. The effects may be mediated through decreased feed intake or through the stress- induced lipolysis pathways. Pen moves result in observed social disorder for two days, with a milk yield depression of 2 to 5 percent for the average cow. While this is a modest effect, social stress can effect the nondominant cow to a much greater degree.
Dominant cows (usually older, larger, more senior and gaining weight) are largely unaffected by a group change. However, nondominant cows (typically younger, smaller body size and cows losing weight) may be targets of aggressive social behavior, resulting in fewer opportunities for feed and rest.
Clinical ketosis and fat infiltration of the liver in late pregnant cows has been observed following feed restriction of 30 to 50 percent or fasting for four to six days. Therefore, coupling the natural decline in DMI with social stress lasting more than two days, especially in nondominant animals entering a marginal housing situation, a significant proportion of animals could be placed in acute negative energy balance, leading to energy distress and clinical disease.
Social effects are accentuated in larger cow groups or herds, so they assume more importance as herds grow in size. The ability to measure cow interaction, and the effect it has on feeding behavior, is only beginning to be addressed. Social interaction is dependent on the constitution of the group, as well as housing, feeding and other environmental factors. Therefore, the relationships can become complex and difficult to predict. In general, minimizing regrouping at key times has been under investigation. These times include the period of five days prior to calving and one to 10 days after calving.
Relationships of energy, disease and host defense
Three other related diseases, retained placenta, endometritis and mastitis, are prevalent conditions that have been putatively associated with energy deficiency in cows. Endometritis and mastitis affect 17 percent and 13 to 45 percent of lactations, respectively, and are infectious in origin, but the bacterial agents are considered opportunists, so these diseases are largely determined by cow defense.
Neutrophils are very important in bacterial defense, and it was shown that neutrophil function declines in late gestation, reaching a nadir near calving. Additionally, neutrophils are important in placental release, and cows with retained placenta had a deficiency in neutrophil function in the prepartum period. Ketone bodies appear to decrease neutrophil response.
Cows that exhibited hepatic lipidosis (a lesion consistent with energy distress) took longer to clear experimental intramammary infection and had blunted response to vaccination. In addition, in vivo work suggests improvements in energy balance in late gestation tended to decrease retained placenta.
While it is unclear how negative energy balance affects host defense, it is important to recognize that diseases of the mammary gland and uterus may be associated with energy distress. Energy balance should be considered a potential contributor to these energy-related diseases if antioxidant vitamins and minerals are adequate.
Metabolic diseases are interrelated so that one disease increases risk for another. The energy-associated diseases include ketosis, displaced abomasum, fatty liver, retained placenta, metritis and possibly mastitis. The root cause of these conditions is an energy distress situation, where cows respond inappropriately to the negative energy balance of early lactation. It is likely the negative energy balance of early lactation will be accentuated as milk production rises.
Providing an environment for an adaptive cow response will remain key to health. Dairy advisers must take an active role in promoting quantitative monitoring to assist the producer. In addition to tracking average DMI, monitoring energy balance using milk or blood NEFA or ketone assays may be essential and may provide an early warning of problems to come.
Since disease represents failures (those cows who could not negotiate stress), analysis of disease incidence records must be conducted and compared to known risk factors, including BCS, DMI, pen moves and concurrent disease. These areas are obvious points where nutritionists and veterinarians can interact in a cooperative relationship. PD
References omitted due to space but are available upon request.
—From 2005 Tri-State Dairy Nutrition Conference Proceedings
William B. Epperson, Department of Veterinary Preventive Medicine, Ohio State University