title: Milk fever in dairy cows: a review of pathophysiology and control principles.
abstract: The periparturient or transition period of 4 weeks before and 4 weeks after calving is characterised by a greatly increased risk of disease. Hypocalcaemia around calving is a risk factor for many of these diseases and is an indirect risk factor for increased culling. The incidence of clinical hypocalcaemia (milk fever) in the field generally ranges from 0-10%, but may exceed 25% of cows calving. In research trials conducted on milk fever the incidence has approached 80% of cows calving. Homeostasis of calcium (Ca) is regulated by calcitonin, parathyroid hormone and 1,25(OH)(2) vitamin D(3). Age increases the risk of milk fever by approximately 9% per lactation. Control of milk fever has revolved around stimulation of homeostatic mechanisms through feeding a pre-calving diet low in Ca. More recently, the role of the dietary cation anion difference (DCAD) in the prevention of Ca disorders has been examined, both by field research and meta-analysis. The most appropriate form of the DCAD equation has been contentious, but recent meta-analyses have shown that the equation (Na(+)+K(+))-(Cl(-)+S(2-)) is most effective for predicting milk fever risk. Decreased risk of milk fever is linear with DCAD, whereas the effect of DCAD on urinary pH is curvilinear. A pivotal role of providing dietary magnesium (Mg) before calving has been confirmed by meta-analysis, and a quadratic effect of Ca on milk fever risk was found with a peak occurring with dietary levels of 1.1-1.3% of dry matter. Risks of milk fever increase with increased dietary phosphorus (P) fed pre-calving and with increasing days of exposure to a pre-calving diet. Meta-analysis has revealed that the important roles of dietary Ca, Mg and P, as well as the duration of exposure to the pre-calving diet in milk fever control strategies are independent of DCAD. Studies on the effect of exposure to well designed pre-calving diets have shown that substantial improvements in production, reproduction and animal health can be made but further examination of the influence of the period of exposure to different diets is warranted.
authors.affiliation: Bovine Research Australasia, Camden 2570, Australia; University of Sydney, Camden 2570, Australia.
authors.forename: Peter J
authors.initials: PJ
authors.lastname: DeGaris
authors.forename: Ian J
authors.initials: IJ
authors.lastname: Lean
mesh_terms: D000367:Age Factors; D000821:Animal Feed / Q000009:adverse effects*; D000824:Animal Nutritional Physiological Phenomena; D000818:Animals; D002136:Calcium, Dietary / Q000008:administration & dosage; D002417:Cattle; D002418:Cattle Diseases / Q000453:epidemiology* / Q000209:etiology / Q000517:prevention & control; D005260:Female; D006996:Hypocalcemia / Q000453:epidemiology / Q000209:etiology / Q000517:prevention & control / Q000662:veterinary*; D008274:Magnesium / Q000008:administration & dosage; D009751:Nutritional Requirements; D010319:Parturient Paresis / Q000453:epidemiology* / Q000209:etiology / Q000517:prevention & control; D016226:Phosphorus, Dietary / Q000008:administration & dosage; D011247:Pregnancy; D012307:Risk Factors
chemical_list: D002136:Calcium, Dietary; D016226:Phosphorus, Dietary; D008274:Magnesium