Acta veterinaria Scandinavica. Supplementum最新文献

The term "Production Diseases" referred traditionally to those diseases induced by management practices, metabolic diseases are typical examples. Recently, the term "Production related diseases" has been enhanced to include other traits, such as infertility, and diseases such as mastitis and lameness that might involve infectious agents but exacerbated by nutritional or managemental factors. The presentation deals with Production Diseases in the context of integrated herd health programs, using periparturient diseases and traits as an example. Studies, based on 9377 lactations of cows calving in the period 1995 through 1998 from the author's practice in 7 Israeli Holstein herds, show that most periparturient diseases and traits are followed by increased culling, lower production associated with late peaks and lower persistency, and impaired fertility. The effects are independent of other diseases, and at times are long lasting. Production Diseases are often multifactorial and appear at the same stage of lactation. Independent relationships among them must be established, so that common cause effects, direct and indirect causal associations, and incidental relationships can be differentiated. Control of Production Diseases often involves various disciplines and therefore calls for a "multivariate approach". Such an approach, centered on the herd, has led to the adaptation of integrated programs for herd health. The programs are characterized by the adaptation of multidisciplinary, multifactorial, and a population approach to clinical entities. Preventive measures and routine examinations are the hard core of programs, but deeper involvement in nutrition, production and economics is called for. A routine monitoring and causal analysis of periparturient traits and diseases, production, fertility and abortions are carried out, relevant data are processed, and monitoring reports are issued routinely. Five different linear regression models evaluate factors responsible for losses of a) peak milk yield; b) economy corrected (ECM) peak milk yield; c) extended 305-d milk yield; d) daily 3.5% FCM in the first 90 days in milk; and e) persistencies. Three different logistic and linear regression models evaluate factors that contribute to a) "non pregnancy to first service"; b) unobserved heat; and c) open days. Narrowing down the field of investigation is essential for an intervention to be efficient. Conclusions are drawn from the epidemiological study and the proposed recommendations are weighed with cost/benefit considerations. Possible losses are quantified and used with expected return value in decision analysis. Production Diseases are at times the outcome of managemental mistakes brought about by the drive for higher yields. Integrated herd health programs help to control the negative effects of management by enhancing production under optimal feeding and management regimens. The estimated contribution of improved management to the Israeli natio

Hypocalcaemia or milk fever is a condition resulting from an insufficiency of plasma calcium to maintain proper body function and is probably the most prevalent mineral-related disorder faced by the transition cow. It is also referred to as parturient paresis or parturient paralysis due to the recumbency that accompanies the most common hypocalcaemia, that is hypocalcaemia that occurs at or around calving. Milk fever was first reported in Germany in 1793 and since then has been the study of many researchers because of its economic importance, reducing milk production by 7 to 14%, depending on the degree of severity. Its prevention has been addressed by different methods including deliberately changing the blood acid-base balance through supplementation of metabolically strong anions (chlorine and sulphur) in an attempt to improve calcium homeostasis in the periparturient cow. This adjustment to the systemic acid-base balance of the cow is difficult to achieve practically and consistently in pasture-based systems and recent research has questioned its efficacy in maintaining a periparturient eucalcaemia.

The background to the development of a novel concept for the prepartal activation of calcium absorption capacity as a means of preventing parturient hypocalcaemia and milk fever in grazing ruminants is described. It was hypothesised that this objective could be achieved by decreasing the bio-availability of calcium from pasture for a 3 week period. Soya bean oil was chosen as a supplement, from a number of potential binding agents, to form poorly digestible calcium soaps in the gastrointestinal tract. 28 mature twin-pregnant ewes in late pregnancy were used as assay animals to test the hypothesis, and they proved to be a sensitive experimental model for dairy cows. Following the treatment period, overnight starvation was used to challenge calcium homeostasis. Calcium absorption capacity was assessed indirectly by measuring strontium concentrations in plasma following oral dosing with strontium chloride. Strong support for the hypothesis was obtained as the 14 Treated ewes were protected from severe fasting-induced hypocalcaemia (P = 0.002), and this was associated with a greatly increased capacity of the ewes to absorb calcium. The feeding strategy developed in this experiment led to the production of a Calcigard concentrate supplement which was subsequently shown to protect cows from hypocalcaemia and milk fever, and stimulate production.

The objective of the present study was to monitor serum and urine biochemical changes in dairy cows during and after oral administration of a synthetic sodium aluminium-silicate (zeolite A). A prospective longitudinal study involving four non-pregnant and non-lactating cows was chosen. Cows were randomly allocated to either a control or experimental group. The period of observation was three weeks. During the first week (period 1) cows were maintained on basic ration for the purpose of recording baseline values. During the second week (period 2) control cows were fed a basic diet (grass silage), while cows in the experimental group were fed the basic diet and supplemented with 1 kg zeolite pellets once daily. During the third week (period 3) both groups were fed the basic ration only and observed for any persistent effects after zeolite withdraw. Daily sampling included blood and urine. Selected physiological parameters were compared between groups during period 2 and 3, whereas mean values from period 1, 2 and 3 were compared within the groups. Zeolite supplementation revealed a significant influence on calcium homeostasis. A slight decrease in serum Ca and in renal excretion of calcium was observed in the experimental group at initiation of supplementation, whereas an increment in these parameters was recorded after withdrawal of zeolite supplementation. It is assumed, that zeolite caused a reduction in the availability of dietary calcium during supplementation, which possibly elicited an activation of calcium mobilisation. The influence of zeolite on calcium homeostasis was not evident from monitoring serum concentration of calcium regulating hormones (PTH, 1,25(OH)2D3, 25(OH)VitD) or renal excretion of markers of bone resorption. Enhanced active intestinal calcium absorption and bone resorption was therefore considered insignificant in the calcium mobilisation under the conditions of this experiment. The origin of the increased amount of Ca, which was observed in serum and urine after zeolite withdraw, is at present unknown, but it is suggested, that the readily mobilized Ca-pool in bone was a contributing factor. An effect of zeolite on phosphate and magnesium homeostasis in the experimental group was evidenced from the values of serum concentration and fractional excretion, which during supplementation were significant lower than in the control group. The influence of zeolite on phosphorus and magnesium is presumed to result from a combination of interference of zeolite with intestinal absorption and a marginal dietary supplementation of these minerals.

Disodium EDTA is a chelating agent used in studies involving calcium. The sodium ion of the chelate is displaced by calcium to form soluble, non-toxic physiologically unavailable complexes that are excreted through urine. When EDTA binds the available calcium in the blood, an animal is forced into a state of negative calcium balance, a situation that mimics the principle of lowering dietary calcium in preventing milk fever. Although limited evidence is available, it is likely that calcium homeostatic mechanisms respond under such circumstances through the effect of parathyroid hormone and 1,25(OH)2 vit D3 on bone, gastrointestinal tract and the kidney. Investigations involving milk fever prevention by dietary manipulation using EDTA-induced hypocalcaemic or milk fever cow models should be interpreted with caution because EDTA is thought to be invasive to calcium homeostatic mechanisms.