Most of the metabolic diseases of dairy cows-milk fever, ketosis, retained placenta, and displacement of the abomasum-occur within the first 2 wk of lactation. The etiology of many of those metabolic diseases that are not clinically apparent during the first 2 wk of lactation, such as laminitis, can be traced back to insults that occurred during early lactation. In addition to metabolic disease, the overwhelming majority of infectious disease, in particular mastitis, becomes clinically apparent during the first 2 wk of lactation. Three basic physiological functions must be maintained during the periparturient period if disease is to be avoided: adaptation of the rumen to lactation diets that are high in energy density, maintenance of normocalcemia, and maintenance of a strong immune system. The incidence of both metabolic and infectious diseases is greatly increased whenever one or more of these physiological functions are impaired. This paper discusses the etiological role of each of these factors in the development of common diseases encountered during the periparturient period.

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The stress of parturition in the dairy cow is associated with increased susceptibility to infectious disease. During the periparturient period the demands for calcium are increased; these increased demands for calcium can result in subclinical or clinical hypocalcemia. Periparturient cows also experience significant immune suppression. Because intracellular calcium signaling is a key early feature in immune cell activation, we have hypothesized that the increased demand for calcium in periparturient cows may adversely affect intracellular calcium stores of immune cells. This reduction in intracellular calcium stores in immune cells could blunt intracellular calcium release following an activating stimulus, contributing to the immune suppression seen in these animals. To test this hypothesis, peripheral mononuclear cells were obtained from 27 multiparous dairy cows spanning a period of 2 wk before and 2 wk after parturition. Following activation of these cells by anti-CD3 antibodies plus secondary antibodies, intracellular calcium release from intracellular stores was measured. The intracellular calcium released in response to the activation signal declined as calcium demand for lactation became more intense and recovered as plasma calcium normalized. Intracellular calcium stores in peripheral mononuclear cells, estimated by pretreating cells with pervanadate and ionomycin, significantly decreased at parturition and returned to normal levels as the cows' blood calcium returned to normal levels. Hypocalcemia, which is common in periparturient dairy cows, is associated with decreased intracellular calcium stores in peripheral mononuclear cells. Our data suggest that this is the cause of a blunted intracellular calcium release response to an immune cell activation signal. It is concluded that intracellular Ca stores decrease in peripheral blood mononuclear cells (PBMC) before parturition and development of hypocalcemia. This suggests that systemic calcium stress precedes measurable hypocalcemia, particularly in cows that will develop milk fever. Therefore, PBMC intracellular Ca stores are a more sensitive measure of calcium stresses in transition cow. This decrease in PBMC intracellular Ca stores before parturition and the development of hypocalcemia contributes to periparturient immune suppression.

Milk fever is a complex metabolic disorder that occurs at the onset of lactation. Clinical symptoms of this disease include inappetence, tetany, inhibition of urination and defecation, lateral recumbency, and eventual coma and death if left untreated. The hallmark of this disease is severe hypocalcemia, which probably accounts for most of the clinical signs associated with a milk fever episode. Several factors have been consistently associated with increased incidence of milk fever, including parturition and initiation of lactation, advancing age, breed, and diet. Of the various methods used in attempts to control the disease, the most progress has been made in dietary management. Until recently, most attention has focused on manipulating the levels of dietary calcium to control milk fever incidence; results, however, have been inconsistent, except for those diets containing very low (8 to 10 g/d) concentrations of Ca. During the past decade, there has been renewed interest and research in the use of dietary anions (Cl- and SO4(2-) in controlling milk fever. An outgrowth of this research has been the surprising realization that dietary K is significant (perhaps more significant than Ca) in determining the susceptibility of dairy cows to milk fever. This knowledge has expanded the understanding of the pathogenesis of milk fever and has focused attention on research designed to study methods for neutralizing the detrimental effects of dietary K excess on periparturient animal health. This report discusses various practical strategies and potential research areas for managing the dietary forage components to minimize the effects of K on milk fever incidence.

It is unclear why some cows fail to expel the placenta following calving. One theory suggests the fetal placenta must be recognized as "foreign" tissue and rejected by the immune system after parturition to cause expulsion of the placenta. We hypothesized that impaired neutrophil function causes retained placenta (RP). We examined the ability of neutrophils to recognize fetal cotyledon tissue as assessed by a chemotaxis assay, which utilized a placental homogenate obtained from a spontaneously expelled placenta as the chemoattractant. Neutrophil killing ability was also estimated by determining myeloperoxidase activity in isolated neutrophils. Blood samples were obtained from 142 periparturient dairy cattle in two herds. Twenty cattle developed RP (14.1%). Neutrophils isolated from blood of cows with RP had significantly lower neutrophil function in both assays before calving, and this impaired function lasted for 1 to 2 wk after parturition. The addition of antibody directed against interleukin-8 (IL-8) to the cotyledon preparation used as a chemoattractant inhibited chemotaxis by 41%, suggesting that one of the chemoattractants present in the cotyledon at parturition is IL-8. At calving, plasma IL-8 concentration was lower in RP cows (51 +/- 12 pg/ml) than in cows expelling the placenta normally (134 +/- 11 pg/ml). From these data, we suggest that neutrophil function is a determining factor for the development of RP in dairy cattle. Also, depressed production of IL-8 may be a factor affecting neutrophil function in cows developing RP.

The Journal of Dairy Science has increasingly become a primary outlet for scientific research concerning the health of the dairy cow and her calf. This paper attempts to highlight Journal of Dairy Science articles that have linked nutrition and nutritional strategies to reduce disease incidence on the dairy farm. Disorders associated with an animal's inability to cope with the demands of high production include diseases such as milk fever and ketosis, which clearly are related to the cow's inability to maintain bodily functions in the face of negative calcium or energy balance. Improved nutrition of the late gestation cow can reduce the incidence of some of these disorders. Susceptibility to infectious disease is dependent on the integrity of the immune system, and recent studies have shed light on nutritional factors that affect leukocyte function. Other disorders, such as retained fetal membranes, udder edema, and displacement of the abomasum are not easily categorized as to their cause, but nutritional strategies have been developed to help prevent these disorders as well.