Poisoning In Cattle Research Articles

Lantana poisoning of cattle and sheep in New Zealand

The investigation of a field case of Lantana camara poisoning in cattle is reported. Toxicity was confirmed by the experimental dosing of two sheep with dried leaf powder at 6 and 12 mg/kg body weight. Marked cholestatic hepatophy and renal tubular disease resulted. This is the first reported case of toxicity due to grazing a Lantana camara variety grown in New Zealand.

Organomercuric poisoning in fat cattle.

Organomercuric poisoning in fat cattle.

Suspected hydrocyanic acid poisoning in cattle.

Suspected hydrocyanic acid poisoning in cattle.

The occurrence, cost and control of sawfly larval (Lophyrotoma interrupta) poisoning of cattle in Queensland 1972-81.

A postal survey of cattle producers in the Maranoa, Warrego and Leichhardt districts of Queensland where poisoning of cattle by larvae of the sawfly (Lophyrotoma interrupta) occurs was carried out in 1982 with 179 replies (64% of those contacted). During 1972-81, 50 farms with 84,300 cattle experienced deaths (5254 on 37 farms) during July to September. The worst years were 1975 (955 deaths) and 1979 (1895 deaths). Heavy losses occurred on 9% of farms. These were where the silver-leaved iron bark (Eucalyptus melanophloia) was most common. To prevent the disease, 37 graziers moved cattle from dangerous areas and 52 partly removed E. melanophloia from their farms. 31 fed supplements to try to prevent the pica thought to cause cattle to eat larvae. 53 who had suffered sporadic or no deaths took no action. The survey results indicated that cattle should not be returned to dangerous areas until early October. The estimated total yearly cost from reduced carrying capacity, control measures and deaths was $1,100,000 (1981 values). Improved control by advice on property management and a better knowledge of the population dynamics of the sawfly was suggested. The use of antidotes or toxoids was thought inappropriate.

Acute lead poisoning in beef cattle

Lead Poisoning in cattle is possibly one of the most commonly diagnosed intoxications. Lead toxicosis in cattle may present as a neurological or intestinal syndrome and may be subacute, acute, or chronic. Sources of lead are variable and include oils, paints, lead batteries, and lead shot. Frequently the source of lead is undetermined.
 In this unique report, we describe an acute outbreak of lead poisoning (ALP) in cattle which was traced to a discarded tractor battery. In addition, insurance liability claims are discussed and presented.

Administration of activated charcoal for the treatment of lantana poisoning of sheep and cattle.

The use of activated charcoal for treating lantana poisoning was investigated. When 500 g of activated charcoal was given orally with toxic Lantana camara, it protected sheep against intoxication. Administration to sheep of 500 g of activated charcoal in 4 1 of electrolyte solution orally 6 days after the onset of lantana poisoning and then 4 1 of electrolyte solution the next day, was followed by recovery from the intoxication. Mortality was significantly higher in intoxicated sheep given only the electrolyte solution and in untreated sheep. Six cows with naturally occurring lantana poisoning were treated with 2-2.5 kg of charcoal in 20-30 1 of electrolyte solution given by stomach tube and all the animals recovered. It is recommended that sheep with lantana poisoning be treated orally with 500 g of activated charcoal in 4 1 of electrolyte solution, and that cattle be given 2 kg of charcoal in 20 1 of electrolyte solution. Supportive treatment for photosensitization and dehydration may also be required.

Cestrum parqui (green cestrum) poisoning in cattle.

Naturally occurring cases of poisoning of cattle by Cestrum parqui were characterised by ataxia, depression, recumbency, convulsions and death. Three cattle were dosed experimentally by intrarumenal administration of fresh plant material. One calf died 48 h after receiving 30 g (wet weight) of plant/kg bodyweight. Doses of 11 and 17 g/kg caused only mild intoxication, with dullness and anorexia lasting 2 days. In natural and experimental cases the main lesion was hepatic periacinar necrosis. Elevated levels of plasma aspartate transaminase and prolonged prothrombin times were demonstrated in experimental cases. Haemorrhage beneath the serosa and into the intestinal lumen occurred in field cases, but not in the experimental. It is concluded that C. parqui poisoning in cattle is a primary hepatotoxicity.

Sodium monochloroacetate poisoning of cattle and sheep.

Two separate incidents of poisoning, one involving the death of 10 cattle and the other four sheep following the use of sodium monochloroacetate, were investigated. The cattle drank from a farmyard drain overflow which undissolved herbicide entered. Sheep had access to spilt herbicide by a standpipe. Sodium monochloroacetate appears to be equally toxic to both sheep and cattle. The need to follow the manufacturers' instructions is emphasised.

Poisoning of cattle by Glyceria maxima.

Australian Veterinary JournalVolume 60, Issue 7 p. 220-221 Poisoning of Cattle by Glyceria maxima N. J. BARTON, N. J. BARTON Regional Veterinary Laboratory, Department of Agriculture, P.O. Box 483, Bairnsdale, Victoria 3875Search for more papers by this authorS. McORIST, S. McORIST Regional Veterinary Laboratory, Department of Agriculture, P.O. Box 483, Bairnsdale, Victoria 3875Search for more papers by this authorD. S. McQUEEN, D. S. McQUEEN P.O. Box 378, Warragul, Victoria 3820Search for more papers by this authorP. F. O'CONNOR, P. F. O'CONNOR 59 Bair Street, Leongatha, Victoria 3953Search for more papers by this author N. J. BARTON, N. J. BARTON Regional Veterinary Laboratory, Department of Agriculture, P.O. Box 483, Bairnsdale, Victoria 3875Search for more papers by this authorS. McORIST, S. McORIST Regional Veterinary Laboratory, Department of Agriculture, P.O. Box 483, Bairnsdale, Victoria 3875Search for more papers by this authorD. S. McQUEEN, D. S. McQUEEN P.O. Box 378, Warragul, Victoria 3820Search for more papers by this authorP. F. O'CONNOR, P. F. O'CONNOR 59 Bair Street, Leongatha, Victoria 3953Search for more papers by this author First published: July 1983 https://doi.org/10.1111/j.1751-0813.1983.tb09591.xCitations: 4AboutPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL Share a linkShare onFacebookTwitterLinked InRedditWechat No abstract is available for this article.Citing Literature Volume60, Issue7July 1983Pages 220-221 RelatedInformation

Outbreak of monensin poisoning in cattle.

Following accidental overdosage with monensin, nine deaths occurred in a batch of 40, four-to-seven-month-old calves. A description of the incident is given including the findings on post mortem examination. Inaccurate on-farm feed mixing can present problems as was highlighted by this outbreak.

Nitrate poisoning in cattle. 7. Prevention.

Results are summarized from 44 feeding trials with dry or lactating cows fed hay, pre-wilted grass silage or freshly mown grass with or without concentrates. As nitrate content of the forage increased, the moment at which the highest methaemoglobin (MHb) concentration occurred was delayed. As the MHb peak increased, more time was required to reduce MHb to normal values of 2-3%. Dry matter (DM) intake varied with type of forage. Consumption of 1.1 kg DM/100 kg bodyweight required 2 hours with hay or silage and 3.5 h with fresh grass. The relationship between nitrate intake and the formation of MHb in the blood was used to calculate the amount of forage that may be consumed per meal without causing symptoms of nitrate poisoning. Hay and pre-wilted silage with a nitrate content of up to 0.75% in the DM may be given ad lib. Indoor feeding of freshly mown grass with a nitrate content of up to 1.5% may also be given with restriction. Under grazing conditions, grass with a nitrate content of 2% in DM was safe without restriction. Nitrate poisoning may also be prevented by inhibiting nitrate reduction in the rumen by a daily dose of tungsten (wolfram). However, all potential hazards of this prophylactic treatment need to be examined before its use under practical conditions can be recommended. (Abstract retrieved from CAB Abstracts by CABI’s permission)

Acute bracken poisoning in homogastric and ruminant animals

SynopsisThe toxicity of bracken fern (Pteridium aquilinum(L) Kuhn) is complicated because this plant elaborates more than one type of agent potentially harmful to livestock.When simple-stomached animals are fed a diet containing some green fronds or rhizomes for a few weeks, they develop anorexia and inco-ordination symptoms; this polyneuritic syndrome shows all the characteristics of thiamine deficiency. Thiamine therapy is effective in curing the animal provided it is administered at the onset of clinical symptoms.Bracken staggers in the horse and rhizome poisoning of pigs are diseases of this nature,i.e. an avitaminosis B1has been induced. The causative agent in the fern is a steam-labile enzyme, thiaminase I, which destroys thiamine in such a way that it is no longer active in animal nutrition.Acute cattle bracken poisoning occurs after frequent eating of the fern over a period of weeks.Haemorrhages and fever are the characteristic clinical symptoms, and the animal usually dies within a few days. The fundamental lesion is bone marrow aplasia resulting in a severe leucopenia and thrombocytopenia.Thiaminase I is not involved in this disease. Bracken contains an organic chemical(s) which poisons rapidly dividing cells in the bovine animal. Sheep are less sensitive to this toxic agent, although the condition has been described along with 'bright-blindness* in some parts of Britain (e.g. North York Moors).Purification of the active principle causing cattle bracken poisoning from green fronds and rhizomes is far advanced; these methods are described, along with calf toxicity tests on each fraction. Chemical investigations are also under way to determine the nature of the components.Whether the cattle factor, in small doses over an extended period of time (years), is also the agent causing tumours in livestock, is probable but not certain. Some bracken constituents shown to be carcinogenic in small animals, e.g. shikimic acid, quercetin or the tannin fraction, are not capable of producing acute cattle bracken poisoning; neither does safrole or 1-indanone.Some of the sesquiterpene glycosides—the 'pterosides' and/or their aglycones, the 'pterosins', of which over 30 have been identified in bracken—are likely candidates. On the other hand, the active principle(s) may be something quite different; the search continues.

Insects Associated with Broom Snakeweed [Xanthocephalum sarothrae] and Threadleaf Snakeweed [Xanthocephalum microcephala] in West Texas and Eastern New Mexico

Insects Associated with Broom Snakeweed [Xanthocephalum sarothrae] and Threadleaf Snakeweed [Xanthocephalum microcephala] in West Texas and Eastern New Mexico

Disulphide exchange reactions in the control of enzymic activity. Evidence for the participation of dimethyl disulphide in exchanges.

The causative agent in kale poisoning of cattle is the disulphide, dimethyl disulphide. Typical signs of kale poisoning are circulating dimethyl disulphide in the blood, Heinz body (deposits of methaemoglobin) formation in the erythrocytes and loss of body weight. Experiments in vitro have demonstrated that dimethyl disulphide can participate in disulphide exchange reactions which have a controlling role on proteolytic enzymes. We chose the enzyme trypsin, the active centre of which is maintained by a significant disulphide bond and the enzyme papain which is a thiol protease, to illustrate the mechanisms involved in these disulphide exchange reactions.

Thiamin (vitamin B 1) effects on lead intoxication and deposition of lead in tissues: Therapeutic potential

The purpose of this study was to evaluate the effects of thiamin on lead (Pb) poisoning in cattle. Fifteen Holstein male calves were divided into three groups: Group I served as controls, Group II calves were dosed orally with 5 mg Pb acetate/day/kg of body wt, and Group III calves were dosed similarly with Pb and with 100 mg/day/calf of thiamin hydrochloride, subcutaneously. Calves were treated daily for 20 days. None of the control or Pb plus thiamin-treated calves showed clinical signs of poisoning and no deaths occurred. However, four of five Pb-treated calves showed signs of Pb poisoning and two died during the study. Tissues from both groups receiving Pb contained significantly higher ( p < 0.01) concentrations of Pb than tissues from control calves. However, tissues from calves receiving Pb plus thiamin contained 2 to 10 times less Pb than tissues from calves receiving only Pb. The Pb concentrations in liver, kidney, and blood from thiamin-treated calves remained below confirmatory levels associated with Pb poisoning; while Pb concentrations in the same tissues from calves dosed only with Pb were within the range considered diagnostic of Pb poisoning. On the other hand, δ-aminolevulinic acid dehydratase activity in erythrocytes was decreased 70% from pretreatment levels in both groups receiving Pb. Thus, thiamin appeared to have no protective effect on the ability of Pb to inhibit this enzyme. But in the tissues analyzed, thiamin interacted with Pb in some way to prevent tissue accumulation, thus preventing clinical signs and death. These results suggest that therapeutic doses of thiamin may be of value in the prevention and treatment of Pb poisoning in cattle, and in other animals or humans exposed to high environmental levels of Pb.

Nitrate poisoning in cattle. 6. Tungsten (wolfram) as a prophylactic against nitrate-nitrite intoxication in ruminants.

The amount of nitrite formed in the rumen after supply of potassium nitrate was decreased considerably by tungsten, which was administered as sodium tungstate to cows orally and by rumen fistula in daily doses of up to 6.6 mg per kg body weight. This effect of tungsten depends on the molybdenum content of the fodder and can be overcome in the case of high molybdenum levels. The relationship between the nitrate intake of the animal, the dose of tungsten administered to the animal daily and the highest concentration of nitrite reached in the rumen is given as a mathematical equation as well as in the form of a triangular diagram. By means of this three-element relationship and as a result of kinetic studies on the action of tungsten, a dosage pattern of tungsten was elaborated. The effectiveness of tungsten as a protective against nitrate intoxication was proved on cows dosed repeatedly as well as with single doses of nitrate up to 500 mg NO3 per kg body weight. It is concluded finally that tungsten offers a high degree of protection against nitrate toxicity to ruminants. (Abstract retrieved from CAB Abstracts by CABI’s permission)

Investigation of an arsenic poisoning case

After lead, arsenic constitutes one of the most important toxicological hazards to farm animals. Arsenic is rather ubiquitous in nature, and trace or background levels can be found normally in nearly all animal and plant tissues. Arsenical compounds have been used for a variety of purposes, including for treatment of disease, as feed additives to promote weight gains, and as herbicides, cotton defoliants and appetite stimulants.&#x0D; Toxicity varies with the species of animal exposed, the formulation of the arsenical, the route of exposure, and factors affecting rate of metabolism and excretion. It has long been known that most animals except the rat and man rapidly excrete arsenic.&#x0D; Arsenic poisoning in cattle is manifested by acute or subacute syndrome, and chronic poisoning has not been clearly documented. Veterinary diagnostic laboratories have found that if an animal survives the acute crisis and lives for several days after consuming a toxic dose of arsenic, then the liver and kidney levels of arsenic may be below levels ordinarily considered diagnostic.&#x0D; The following case emphasizes the need for documenting normal background levels of arsenic and other toxicants in animal tissues.

Nitrate poisoning in cattle

Summary In a series of experiments the effect of administering KNO(2) 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, pO(2), O(2)-saturation, pH, pCO(2), and (NO(2)) 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 O(2)-saturation was calculated from the estimated O(2)-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 NO(2)/kg body weight intravenously or of 30 mg of NO(2)/kg body weight orally to the dam caused much higher MHb percentages and NO(2) contents in the maternal blood than in the foetal blood. In maternal blood the ratio of NO(2) 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 O(2)-saturation dropped simultaneously with the increase in methaemoglobin. Nitrite treatment caused a drop in the maternal blood pressure; heart rate and respiration rate increased. O(2)-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.

Nitrate poisoning in cattle. 5. The effect of tungsten on nitrate formation by rumen microbes.

Sodium tungstate added to rumen fluid depressed the nitrate reductase activity of rumen microbes. The rate of nitrite formation in rumen fluid fell by about 86% if 20 mu mol of Na2WO4 were added per litre. At 100 and 500 mu mol/l no nitrite accumulation was observed. This inhibition was overcome by molybdenum. Experiments in cows confirmed these in vitro findings. Tungsten is suggested as a promising preventative of nitrite intoxication in ruminants. [For Part 3 see VB 50, abst. 5179.] (Abstract retrieved from CAB Abstracts by CABI’s permission)

Nitrate poisoning in cattle. 3. The relationship between nitrate intake with hay or fresh roughage and the speed of intake on the formation of methemoglobin.

For part 2 see NAR/B 48, 238. 3. In 40 feeding experiments during about 5 years dry or lactating Friesian cows weighing 415 to 670 kg and 3 to 8 years old were given diets of hay, grass pellets, turnips or freshly mown grass in 2 meals daily. During experiments blood from the jugular vein was sampled every 15 min. Cows were induced to increase nitrate intake by being given at least 4 meals of roughage rich in nitrate before blood was sampled. There was a positive relation between nitrate intake and methaemoglobin per cent of total Hb but there were differences within and between different roughages in formation of methaemoglobin. With similar nitrate intake and speed of intake, more Hb was converted into methaemoglobin with hay than with freshly mown grass. That was related to the speed at which the nitrate taken with the roughage was released in the rumen as a substrate for the rumen flora. When hay was soaked in distilled water 80% of the nitrate in the cells diffused into the water within 20 min. With turnip and grass chopped to about 1 cm, 30% of the nitrate diffused into the water within 20 min. (Abstract retrieved from CAB Abstracts by CABI’s permission)