The study used field data from a regular herd health service to investigate the relationships between body condition scores or first test day milk data and disease incidence, milk yield, fertility, and culling. Path model analysis with adjustment for time at risk was applied to delineate the time sequence of events. Milk fever occurred more often in fat cows, and endometritis occurred between calving and 20 d of lactation more often in thin cows. Fat cows were less likely to conceive at first service than were cows in normal condition. Fat body condition postpartum, higher first test day milk yield, and a fat to protein ratio of > 1.5 increased body condition loss. Fat or thin condition or condition loss was not related to other lactation diseases, fertility parameters, milk yield, or culling. First test day milk yield was 1.3 kg higher after milk fever and was 7.1 kg lower after displaced abomasum. Higher first test day milk yield directly increased the risk of ovarian cyst and lameness, increased 100-d milk yield, and reduced the risk of culling and indirectly decreased reproductive performance. Cows with a fat to protein ratio of > 1.5 had higher risks for ketosis, displaced abomasum, ovarian cyst, lameness, and mastitis. Those cows produced more milk but showed poor reproductive performance. Given this type of herd health data, we concluded that the first test day milk yield and the fat to protein ratio were more reliable indicators of disease, fertility, and milk yield than was body condition score or loss of body condition score.
The aim of this study was to estimate phenotypic and genetic parameters for body condition scores (BCS) from the Dutch type classification system. Data included 108,809 Holstein (H) and 26,208 Red-and-White (R) heifers from 9701 herds that were scored once during lactation on a 1 to 9 scale (1 = emaciated and 9 = obese). Mean BCS for H and R data were 4.50 and 4.94, respectively. The BCS decreased as the percentage of Holstein genes increased. For both breeds, BCS after calving was about 5.6 and BCS was lowest around wk 11. For H heifers, mean BCS at drying off was about 0.8 lower than BCS at calving, whereas for R heifers BCS was at about the same level as at calving. Variance components were estimated using an animal model including the effects of herd x visit, classifier, age at calving, DIM, and genetic group. The random herd x visit effect explained about 10 to 15% of the phenotypic variation. Heritabilities ranged from 0.24 to 0.38, depending on breed and lactation period. Genetic correlations between BCS observations in bimonthly lactation periods were close to unity, especially for H. It was concluded that BCS data collected by type classifiers can well be used for genetic evaluation and that genetic variation between animals for BCS-change patterns is a small component of the overall variation in BCS.
This study investigated the relationship between oxidative damage and the effect of vitamin E supplementation in blood, milk, and liver tissue in 16 periparturient heifers. The question is whether measurements of oxidative and vitamin E status in blood of a periparturient cow are representative of the total body, given that blood concentrations of both vitamin E and oxidative stress products change around this period. The daily vitamin E intake of the vitamin E-supplemented Holstein-Friesian heifers (n = 8) was 3,000 international units and was started 2 mo before calving; the control heifers (n = 8) were not supplemented. Oxidative damage was determined on the basis of malondialdehyde (MDA) concentrations. Blood was sampled 9 times before calving, on calving day, and twice after calving. Liver biopsies were taken at wk −5, −1, and 2 relative to calving day. Milk was obtained from all heifers immediately after calving, the first 2 milkings and on d 3, 7, and 14 at 0600 h. Serum and liver tissue were analyzed for vitamin E, cholesterol, and MDA; and milk samples were analyzed for vitamin E, MDA, fat, protein, and somatic cell count. The results showed that vitamin E supplements increased both absolute vitamin E concentrations and the ratio of vitamin E to cholesterol in blood and liver tissue. Absolute vitamin E concentration in milk tended to be greater in supplemented cows. Based on the increased MDA blood concentrations at calving, it seems that dairy heifers experience oxidative stress. The effect of vitamin E on MDA differs between the blood, liver, and mammary gland. Vitamin E supplementation could not prevent the increase in blood MDA at calving, but the significantly lower MDA blood concentrations of supplemented cows in the 2 wk after calving suggest that vitamin E has a role in recovery from parturition-related oxidative stress. Vitamin E Received August 9, 2007. Accepted November 25, 2007. 1 Corresponding author: R.J.Bouwstra@vet.uu.nl 977 supplementation reduced oxidative damage in liver, whereas no obvious effect was found on milk MDA concentrations. A strong relationship was found between blood and liver vitamin E and the ratio of vitamin E to cholesterol. Concentrations of MDA in blood and milk were also strongly related. The results show that the relationship between oxidative damage and vitamin E differs within blood, liver tissue, and milk. This implies that oxidative and vitamin E status calculated on the basis of blood values alone should be interpreted with caution and cannot be extrapolated to the whole animal.
A randomized, controlled field trial with dairy cows demonstrated an adverse effect of vitamin E supplementation during the dry period on mastitis incidence in early lactation. This study was conducted on farms with historically high rates of mastitis to investigate the benefit of vitamin E supplementation on udder health; however, the outcome showed an adverse effect. The aim of the study was to evaluate whether daily supplementation of 3,000 IU of vitamin E to dairy cows during the dry period could improve udder health in commercial herds with a high incidence of mastitis. On 5 dairy farms, dry cows were randomly divided into 2 experimental groups: a high and a low group. Both groups received a dry cow mineral mix providing 3,000 or 135 IU of vitamin E/cow per day, respectively, between dry-off and calving for a mean period of 8 wk. Providing 3,000 IU of vitamin E exceeds NRC standards, but this amount has been used in previous studies. The experiment, as well as the majority of the statistical analysis, were carried out blinded. Blood was sampled 3 times before calving and on calving day. Serum was analyzed for vitamin E and cholesterol. Vitamin E and the vitamin E:cholesterol ratio were analyzed as dependent variables in mixed models and Student's t-tests to study trends in time and differences between groups. Relative risk calculation and survival analysis were used to study the effect of supplementation on mastitis incidence in the first 3 mo of lactation. The results showed that vitamin E supplements increased both absolute vitamin E and the ratio of vitamin E to cholesterol in blood. In the high group, significantly more subclinical and clinical cases occurred, showing the same trend on all farms. In this study, an initial vitamin E level at dry off above 14.5 μmol/L was a risk factor for clinical mastitis, suggesting that the vitamin E status at the start of the dry period is important. It is recommended to work out exactly at what threshold vitamin E is harmful for udder health before new trials with high dosages of vitamin E are started. Additionally, further research is required to investigate the mechanism by which vitamin E affects udder health.
Hypophosphatemia is a common finding in periparturient and anorectic cattle. Although the clinical relevance of hypophosphatemia in cattle is uncertain, it has been empirically associated with persistent recumbency, specifically in periparturient dairy cows. The objective of the present study was to determine if transient dietary phosphorus (P) deprivation over a course of 5 wk, by feeding an approximately 40% P-deficient ration to lactating dairy cows, would result in altered muscle function or muscle P metabolism severe enough to present a risk for animal health and well-being. In addition, we wanted to determine the association between the plasma phosphate concentration ([Pi]) and muscle tissue P content to assess to what extent intracellular P deprivation of muscle cells could be extrapolated from subnormal plasma [Pi]. Ten healthy multiparous, mid-lactating dairy cows received a ration with a P content of 0.18% over a period of 5 wk. Following the P-deprivation phase, the same ration supplemented with P to obtain a dietary P content of 0.43% was fed for 2 wk. Blood and urine samples were collected regularly and muscle biopsies were obtained repeatedly to determine the P content in muscle tissue. Function of skeletal and heart muscles was evaluated by electrocardiography and electromyography conducted repeatedly throughout the study. Feeding the P-deficient ration resulted in the rapid development of marked hypophosphatemia. The lowest plasma [Pi] were measured after 9 d of P depletion and were, on average, 60% below predepletion values. Plasma [Pi] increased thereafter, despite ongoing dietary P depletion. None of the animals developed clinical signs commonly associated with hypophosphatemia or any other health issues. Urine analysis revealed increasing renal calcium, pyridinoline, and hydroxypyridinoline excretion with ongoing P deprivation. Biochemical muscle tissue analysis showed that dietary P depletion and hypophosphatemia were not associated with a decline in muscle tissue P content. Electromyographic examination revealed increased occurrence of pathological spontaneous activity in striated muscles after 2 wk of dietary P depletion in several cows, which could be suggestive of neuromuscular membrane instability. No effect on heart muscle activity was identified electrocardiographically. These results suggest that counter-regulatory mechanisms were sufficient to maintain normal muscle tissue P content during transient and moderate P deprivation. Muscle function was not grossly affected, although the increased occurrence of pathological spontaneous activity suggests that subclinical neuropathy or myopathy, or both, may have occurred with ongoing P deprivation. The results presented here indicate that plasma [Pi] is unsuitable for assessing muscle tissue P content in cattle.
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