Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0030552 (paresis)
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Logistic regression was used to investigate the effects of host characteristics, production, and 23 veterinary diagnoses on the risks of two reticuloruminal disorders, ruminal acidosis and traumatic reticuloperitonitis among 61,124 Finnish Ayrshire cows. Lactational incidence risks were .3% for ruminal acidosis and .6% for traumatic reticuloperitonitis. The relative risk of ruminal acidosis was not related to parity, whereas the risk of traumatic reticuloperitonitis decreased with increasing parity. The risk of traumatic reticuloperitonitis was not related to milk yield of individual affected cows in their current or previous lactation (305-d, 4% FCM), whereas the risk of ruminal acidosis increased with current milk yield. Ketosis, early metritis, nonparturient paresis, and acute and chronic mastitis were risk factors for both reticuloruminal disorders. Parturient paresis was a risk factor for ruminal acidosis. Foot and leg problems were risk factors for traumatic reticuloperitonitis. Herd milk yield in the current or previous lactations was not a risk factor for either disorder nor were the two disorders risk factors for each other. Ruminal acidosis, but not traumatic reticuloperitonitis, had significant seasonal variation with the risk being least in summer. The low risk of ruminal acidosis in summer was not due to seasonality of calving.
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PMID:Effect of diseases, production, and season on traumatic reticuloperitonitis and ruminal acidosis in dairy cattle. 225 85

Parturient paresis (milk fever) is a hypocalcemic disorder caused by the onset of lactation in the dairy cow. In most cows a complete recovery follows a single iv calcium treatment to correct the acute hypocalcemia. However, about 20% of cows treated for parturient paresis experience recurring episodes of hypocalcemia (relapses) requiring further treatment. Analysis of plasma from 8 nonrelapsing parturient paretic and 11 relapsing parturient paretic cows revealed differences in plasma 1,25-dihydroxyvitamin D [1,25-(OH)2D] concentrations before and during the development of hypocalcemia. In nonrelapsing cows, plasma 1,25-(OH)2D increased to 4- to 5-fold as plasma calcium concentrations declined during the first stage of parturient paresis. In relapsing cows, decreases in plasma calcium concentrations during the first stage of parturient paresis were accompanied by just a 2- to 2.5-fold increase in plasma 1,25-(OH)2D. Plasma 1,25-(OH)2D eventually increased 4- to 5-fold in the relapsing cows, but this response was delayed 24-48 h compared with the response in the nonrelapsing cows. Plasma PTH concentration profiles were similar in relapsing and nonrelapsing cows, suggesting that renal 25-hydroxyvitamin D 1 alpha-hydroxylase was temporarily refractory to stimulation by PTH in the relapsing cows. In both groups of cows recovery from parturient paresis began about 12-24 h after plasma 1,25-(OH)2D concentrations had increased 4- to 5-fold. These data imply that lack of production of 1,25-(OH)2D is an important factor in predisposing the cow to relapses of parturient paresis and is critical for recovery from the hypocalcemia associated with the onset of lactation.
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PMID:Recurring hypocalcemia of bovine parturient paresis is associated with failure to produce 1,25-dihydroxyvitamin D. 273 59

Parturient paresis (hypocalcemia) is most likely to affect dairy cattle around the time of parturition. It causes progressive neuromuscular dysfunction and flaccid paralysis. Older dairy cows, cows with a history of parturient paresis during a previous lactation, high-producing cows, and cows from the Jersey and Guernsey breeds are at highest risk for developing parturient paresis. Nonparturient hypocalcemia may also occur and is related to events other than parturition, such as severe stress, that temporarily overwhelm the mechanisms of calcium homeostasis. Beef cattle, sheep, and goats are affected less frequently by hypocalcemia than are dairy cows. Because these species are not as stressed for milk production as dairy cattle, nonparturient hypocalcemia makes up a higher proportion of cases in nondairy ruminants. Clinical signs of hypocalcemia in beef cattle, sheep, and goats tend toward hyperesthesia and tetany rather than the classic flaccid paralysis that occurs in dairy cattle with parturient hypocalcemia. Prompt and effective treatment of hypocalcemia helps to reduce the incidence of secondary complications, such as muscle damage or mastitis. The standard treatment regimen of 500 ml of 23 per cent calcium gluconate, administered intravenously, will elicit a favorable response in approximately 75 per cent of recumbent cows within 2 hours of treatment. Relapses following successful initial therapy are common and may be prevented in part by supplementation of intravenous treatment with an additional 500 ml of 23 per cent calcium gluconate administered subcutaneously. Proper nursing care following treatment speeds recovery and reduces the incidence of secondary complications owing to hypocalcemia.
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PMID:Parturient paresis and hypocalcemia in ruminant livestock. 326 54

Dry cow feeding and management were examined for predisposing factors for parturient paresis in 1,983 Holstein cows from New York Dairy Herd Improvement Cooperative records, monthly technician visits to 31 farms, and questionnaires. Variables were estimated transmitting ability, season of calving, lactation number, parturient paresis, estimated potential hours per day of exercise, and estimated nutrient intakes (protein, calcium, phosphorus, and energy) during the preceding dry period. Nutrient intakes were estimated by farmers for the average dry cow (season dependent) in their herd for the early (greater than or equal to 3 wk prepartum) and late portions of the dry period. Intakes were percentages of National Research Council requirements for a 550 kg dry cow in the last 2 mo of gestation. Nutrient intakes were coded by ranking the herds by percentage of each requirement. Codes represented the approximate lower third, middle third, and top third of the herds. Individual cows were assigned their herd nutrition codes by their season of calving. For stepwise discriminant analysis, the group variable was parturient paresis (94 cases, 1,889 controls). As lactation number (most important) and estimated transmitting ability (second most important) increased, incidence of parturient paresis increased. Parturient paresis was reduced with high dietary protein fed during the early stage of the dry period, with low phosphorus and high energy (lead feeding) closer to calving, and with decreased opportunity for exercise. Most cows were overfed calcium, especially in the late stage of the dry period, but calcium intake was not important when phosphorus was low.
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PMID:Epidemiology of parturient paresis: predisposing factors with emphasis on dry cow feeding and management. 672 26

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.
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PMID:Hypocalcaemia and DCAD for the pasture-based transition cow--a review. 1462 97

Milk fever (MF) is a metabolic disease in dairy cows around parturition. The clinical lead sign is muscular paresis leading in severe cases to paralysis of the affected animal. Multiparturient animals of high performing dairy breeds are most likely to be affected and have a high probability of recurrence. An acute drop in blood calcium levels causes the disease when the demand for calcium at the onset of lactation exceeds the ability to replete blood calcium levels through mobilization from bone and intestinal uptake. With the understanding of the underlying mechanism, calcium supply management and vitamin D supplementation became prime candidates for MF prevention and therapy. Several strategies have been developed for MF prevention. Application of the active form of Vitamin D, 1,25(OH)2D3, was found to prevent MF effectively. In order to prevent a delayed hypocalcemia, which was occasionally seen after stopping the treatment with 1,25(OH)2D3, a new approach was chosen by applying Solanum glaucophyllum extract (SGE), which contains 1,25(OH)2D3-glycosides, as instant-release (irSGE) in combination with slow-release (srSGE) tablets. In a first study, non-lactating cows were treated with a single bolus of either synthetic 1,25(OH)2D3, irSGE, or srSGE and the results were compared to a control group without treatment. Blood serum levels of 1,25(OH)2D3 (1,25D), calcium (Ca), phosphate (P) and magnesium (Mg) were followed for 11days and the area under the curve (AUC) was calculated. Calcium and phosphate excretion in urine were determined during 15days. While serum concentration of 1,25(OH)2D3 was back to pre-treatment level in the irSGE, srSGE and 1,25(OH)2D3 treated group within 3days, calcium and phosphate levels remained elevated for up to 9days. AUC of serum 1,25(OH)2D3 was 2.89 (1,25D), 3.13 (irSGE) and 4.21 (srSGE) times higher than control. Serum calcium levels were 1.07* (for 1.25D); 1.08* (for irSGE) and 1.12* (for srSGE) times higher than control. Serum phosphate levels were 1.20* (for 1,25D); 1.30* (for irSGE) and 1.41* (for srSGE) times higher than control, with * p<0.05. In a second field study calving cows treated with one bolus containing ir- and sr- tablets of SGE were compared to an untreated control group and to a group treated with 4 boli of commercial calcium salts. As a result, calcium serum levels increased (+19% compared to baseline) around calving after treatment with the single bolus of SGE. The single bolus of SGE lead also to an increase of serum phosphate (+31% compared to baseline). These calcium and phosphate increases were statistically significant (p<0.001) 0-24h after calving compared to the control group and to the group treated with calcium salts. The sample size of the study was too small to draw a conclusion on the effect on MF prevention. In conclusion, application of a single bolus of a SGE extract lead to an increase of serum calcium and phosphate for up to 9days and may thus have the potential to prevent a hypocalcemia and -phosphatemia, an important cause for clinical milk fever.
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PMID:Effects of a sustained release formulation of 1,25-dihydroxyvitamin D3-glycosides for milk fever prevention on serum 1,25-dihydroxyvitamin D3, calcium and phosphorus in dairy cows. 2834 73