Chlorate poisoning in beef cattle

A disease syndrome characterized by hemolysis, methemoglobinemia, methemoglobinuria, and death was observed in a herd of purebred Limousin beef cattle grazing on pasture in November in Alberta. Improper disposal of the nonselective herbicide, sodium chlorate, was identified as the causal agent. Highly variable blood methemoglobin levels reflected differences in herbicide consumption.     

Extruded urea could reduce true protein source in beef cattle diets

Rumen micro‐organisms are capable of producing microbial protein from ammonia and carbon skeleton, and non‐protein nitrogen (NPN) may be one of the sources of ammonia. Alternative source of NPN is the slow release of ammonia sources in which the product is the extrusion of starch with urea. This work aimed to determine the effects on nutrient intake, ingestive behaviour, digestibility, nitrogen balance, ruminal pH, rumen ammonia nitrogen, volatile fatty acids (VFA) and blood parameters with increased levels of extruded urea (50, 60, 70 and 80 g/100 kg of body weight [BW]) in beef cattle diet. Four rumen cannulated crossbred steers with initial mean weight of 336 ± 47 kg in a 4 × 4 Latin square design were distributed. Diets were formulated with 400:600 g/kg roughage:concentrate ratio on dry matter based and provided once per day, being used whole corn silage as roughage. There were no effects on nutrient intake (kg/day), ingestive behaviour, apparent digestibility, nitrogen balance, volatile fatty acid (VFA) and blood parameters in extruded urea treatment groups. Similar results were observed on time spent on feeding, rumination and idleness. There were positive linear effects (p = 0.022) on rumen pH in the time of 8 hr after feeding and also on plasma concentration of the extruded urea levels (p = 0.039); whereas a linear negative effect (p = 0.030) was observed on ammonia nitrogen for the collection time of 2 hr after feeding. Increased levels of extruded urea could maintain nutrient intake, digestibility, ingestive behaviour, rumen pH and blood parameters in normal conditions. In conclusion, we recommend the extruded urea use with values up to 80 g/100 kg BW in confined beef cattle that receive balanced diets with 140 g/kg of crude protein.     

Accidental poisoning of a group of yearling cattle by the organophosphate insecticide trichloronat

Eight yearling cattle were accidentally poisoned with the agricultural organophosphate insecticide trichloronat. One animal showed signs of acute organophosphate poisoning and died. The others showed signs of chronic organophosphate poisoning (organophosphate-induced delayed neuropathy) after 2–3 weeks and one animal died from renal failure at 12 weeks. High levels of trichloronat were measured in fat samples at 6 1/2 weeks. The remaining animals still showed signs of ataxia, possibly due to distal axonopathy, 1 year later but no trichloronat was detected in fat samples at this time.     

Accidental poisoning of a group of yearling cattle by the organophosphate insecticide trichloronat

Eight yearling cattle were accidentally poisoned with the agricultural organophosphate insecticide trichloronat. One animal showed signs of acute organophosphate poisoning and died. The others showed signs of chronic organophosphate poisoning (organophosphate-induced delayed neuropathy) after 2-3 weeks and one animal died from renal failure at 12 weeks. High levels of trichloronat were measured in fat samples at 6 1/2 weeks. The remaining animals still showed signs of ataxia, possibly due to distal axonopathy, 1 year later but no trichloronat was detected in fat samples at this time.     

Accidental colchicine poisoning in a dog

A 14-month-old toy poodle-cross was presented, after ingesting the owner's colchicine medication, with severe gastrointestinal disturbances and in shock. Despite aggressive medical management, the patient was euthanized approximately 24 hours after the ingestion. The clinical features, treatment, and necropsy findings of colchicine poisoning are discussed.     

Effects of ruminal casein and glucose on forage digestion and urea kinetics in beef cattle

Effects of supplemental glucose and degradable intake protein on nutrient digestion and urea kinetics in steers (Bos taurus) given ad libitum access to prairie hay (4.7% CP) were quantified. Six ruminally and duodenally cannulated steers (initial BW 391 kg) were used in a 4 × 4 Latin square with 2 extra steers. Treatments were arranged as a 2 × 2 factorial and included 0 or 1.2 kg of glucose and 240 or 480 g of casein dosed ruminally once daily. Each period included 9 d for adaptation, 4 d for total fecal and urine collections, and 1 d for ruminal and duodenal sampling. Jugular infusion of (15)N(15)N-urea with measurement of enrichment in urine was used to measure urea kinetics. Glucose reduced forage intake by 18% (P < 0.01), but casein did not affect forage intake (P = 0.69). Glucose depressed (P < 0.01) total tract NDF digestion. Glucose supplementation decreased ruminal pH 2 h after dosing, but the effect was negligible by 6 h (treatment × time; P = 0.01). Providing additional casein increased the ruminal concentration of NH(3), but the increase was less when glucose was supplemented (casein × glucose; P < 0.01). Plasma urea-N was increased (P < 0.01) by additional casein but was reduced (P < 0.01) by glucose. Microbial N flow to the duodenum and retained N increased (P ≤ 0.01) as casein increased, but neither was affected by glucose supplementation. Urea-N entry rate increased (P = 0.03) 50% with increasing casein. Urinary urea-N excretion increased (P < 0.01) as casein increased. The proportion of urea production that was recycled to the gut decreased (P < 0.01) as casein increased. Glucose supplementation decreased (P < 0.01) urinary urea excretion but did not change (P ≥ 0.70) urea production or recycling. The amount of urea-N transferred to the gut and captured by ruminal microbes was less for steers receiving 480 g/d casein with no glucose than for the other 3 treatments (casein × glucose interaction, P = 0.05), which can be attributed to an excess of ruminally available N provided directly to the microbes from the supplement. Overall, the provision of supplemental glucose decreased forage intake and digestibility. Increasing supplemental casein from 240 to 480 g/d increased urea production but decreased the proportion of urea-N recycled to the gut.     

Nitrate poisoning in cattle

Summary

In a series of experiments the effect of administering KNO₂ was studied, during parturition, on the capability of oxygen transport of maternal blood and on oxygen transfer to foetal blood. The following blood parameters were analysed, MHb percentage, pO₂, O₂‐saturation, pH, pCO₂, and (NO₂) in maternal arterial blood (carotid art.) and venous blood (jugular vein) and in foetal arterial blood (umbilical art.) and venous blood (umbilical vein). The relative O₂‐saturation was calculated from the estimated O₂‐saturation by multiplying with the factor Hb (mmol/1) minus MHb (mmol/1), divided by Hb (mmol/1). In addition, blood pressure in the carotid artery, heart rate, and respiration rate in the dam were continuously recorded for some hours.

A dosage of 9 to 12 mg of NO₂/kg body weight intravenously or of 30 mg of NO₂/kg body weight orally to the dam caused much higher MHb percentages and NO₂ contents in the maternal blood than in the foetal blood. In maternal blood the ratio of NO₂ content td MHb percentage was proportional to that in foetal blood. In the arterial blood, MHb percentages were almost as high as in the venous blood. After administering of nitrite, relative O₂‐saturation dropped simultaneously with the increase in methaemoglobin.

Nitrite treatment caused a drop in the maternal blood pressure; heart rate and respiration rate increased. O₂‐saturation in the blood in the umbilical vein was much lower in the animals with nitrite treatment than in those without. These experimental results show clearly that the oxygen capacity of the blood decreases after nitrite treatment. In pregnant cows the oxygen supply to the foetus will be adversely affected after nitrate intake, especially by the lower oxygen transfer via the placenta, though hardly at all by methaemoglobin formation in the foetal blood.

When the oxygen transfer to the foetal blood decreases too sharply, intra‐uterine death and ultimately abortion may result.     

肉牛微量元素铜的营养

铜是人和动物所必需的微量元素,大量的试验研究已证实,铜具有广泛的生物学作用,它与畜禽的生长性能、免疫功能等都有密切的联系。铜的缺乏对畜禽的造血功能、神经系统、骨骼、结缔组织和被毛的生长发育等均会造成不同程度的不良影响。     

Cocklebur poisoning in cattle

Cocklebur poisoning occurred in a herd of cattle in Oklahoma during the month of July. The poisonous dicotyledonary stage of cocklebur plant growth usually occurs during the early spring in Oklahoma. In this instance, dicotyledonary sprouts were in a lowland pasture adjacent to a river. Sprouting and growth occurred after receding water and hot dry weather had created favorable conditions for germination. The diagnosis was made on the basis of the finding of the dicotyledonary stage of plant growth and evidence of the plants having been grazed, as well as the clinical signs, gross necropsy findings, and histopathologic findings in the affected cattle.     

Hip dysplasia in beef cattle

A bilateral hip lameness has been found in young beef bulls of the Hereford, Aberdeen Angus, Galloway and Charolais breeds in the United Kingdom, North America and Australia. The incidence is usually small and sporadic, but up to half of the male animals on one farm may be affected clinically by the time they are one year old. Clinical lameness begins at three months to two years old, and very occasionally up to three years of age; some calves are obviously affected at birth. Aberdeen Angus cattle tend to be affected earlier than other breeds. Clinical evidence of the condition is almost entirely confined to the male.