Bryophyllum pinnatum poisoning of cattle

SUMMARY Two adult cattle died within 48 h of being fed a large amount of Bryophyllum pinnatum plants collected from a house garden. Clinical signs became apparent the day after feeding and included hypersalivation, ataxia, severe cardiac arrhythmia and laboured respiration. The main necropsy findings were acute rumenitis, reduction of bronchiolar lumens and emphysema.     

Curing experimental Bryophyllum tubiflorum poisoning of cattle with activated carbon, electrolyte replacement solution and antiarrhythmic drugs

A slurry of activated carbon (activated charcoal) in electrolyte replacement solution given by stomach tube and antiarrhythmic drugs given parenterally cured 9 of 11 calves dosed 7 to 24 h previously with a lethal amount (20g/kg) of Bryophyllum tubiflorum flower heads. Two of another 4 calves treated 26 to 36 h after dosing with flowers survived. B. tubiflorum toxins are bufadienolides (cardiac glycosides). Activated carbon was effective at a single dose of 5 g/kg. Calves were rehydrated with oral electrolyte replacement solution at 150 ml/kg in divided doses over 24 h. Tachycardia was treated with intravenous lignocaine (200 mg doses) or propranolol (5 mg doses) and atrioventricular block with atropine (0.5 mg/kg).     

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.     

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.     

Lead poisoning in cattle

Lead poisoning is a frequent cause of poisoning in domestic animals. Signs of encephalopathy and gastroenteritis are commonly observed in cattle following lead poisoning. This article discusses the etiology, epidemiology, pathogenesis, clinical signs, diagnosis, postmortem findings, and treatment of lead poisoning in cattle.     

Onion poisoning of young cattle

Eighty-five cattle (calves and yearlings) were allowed 1000 kg of onions (Allium cepa) a day. Signs of poisoning were observed after five days; 22 animals were affected, one fatally. New illnesses continued to occur for five days after the withdrawal of onions from the diet. Clinical signs included inappetance, tachycardia, staggering and collapse, with jaundiced conjunctivae and haemoglobinuria. Haemolytic anaemia with Heinz bodies in the red cells and leucocytosis were demonstrated.     

Selenium poisoning in dairy cattle

An outbreak of chronic selenium poisoning occurred in a mob of 30 Friesian dairy cows. These cows were all autumn calvers on a well-managed dairy farm.     

Moldy sweetclover poisoning in cattle

Some selected clinical and laboratory aspects of moldy sweetclover poisoning in cattle are reviewed. The prothrombin time is preferred when the disease is suspected.

The bleeding time and whole blood clotting time test are also used.

Dicoumarol is not always detectable in the suspected feed which may be due to sampling technique or inaccuracy in the laboratory assay. The most effective treatment is a whole blood transfusion.

Vitamin K₁ (naturally occurring vitamin K) is an effective antidote but too expensive. Vitamin K₃ (synthetic vitamin K) in both the injectable and oral forms are not as effective as K₁ but are used extensively for treatment and prevention. Feeding the suspected feed for two weeks followed by a one week withdrawal successively or by dilution with other feeds will help to reduce the incidence of disease if other feeds are not available.

Suspected feed should not be fed to cattle for at least three weeks before surgery or parturition.

     

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.     

奶牛铅中毒

1　发病情况及流行病学调查1 999年 3月下旬 ,我市某区专业户郑某共养 4头黑白花奶牛 ,其中犊牛 1头 ,泌乳牛 3头。 3月 1 9日开始饲喂玉米秸杆 ,2 2日开始 1头奶牛产奶量下降 1 0 kg,2 3日 1头犊牛不采食 ,2 4日死亡 ;2 5日死亡 2头 ,2 6日死亡 1头。死前体温 3 8.2℃ ,脉搏 5     

Nitrate poisoning in cattle grazing crops

Extract

Although nitrate/nitrite poisoning of cattle, sheep and pigs has been recognized in New Zealand for many years, it has become more widely publicized in the past 2 years owing to the greater prevalence of poisoning and the involvement of hitherto unsuspected crops, notably ‘Grasslands Tama’ ryegrass. In this review, experiences with recent outbreaks of nitrate poisoning are compared with published observations. Throughout this paper the disease will be referred to as nitrate poisoning.     

Benzene hexachloride poisoning in cattle.

Of 174 cattle dipped in an emulsified preparation of benzene hexachloride labeled for plant use, 18 were fatally poisoned. The preparation contained 0.14% active ingredient, gamma isomer of benzene hexachloride (BHC), a normally safe concentration for cattle. Analyses revealed 0.08% gamma BHC in the used dip and 0.5, 7.9, and 198 ppm in liver, kidney, and hairskin specimens, respectively, from a fatally affected cow. Microscopic examination of the freshly prepared dip demonstrated emulsion droplets ranging from 5 to 60 mu in diameter.