猪铜中毒的诊治及其注意事项

1 中毒机理 急性铜中毒是由于猪短期内摄人过量铜盐（多为可溶性硫酸铜），由于大量铜盐具有凝固蛋白和腐蚀作用，从而导致胃肠黏膜出现凝固性坏死。严重者表现为出血性坏死性胃肠炎。慢性铜中毒是由于猪长期摄取少量铜而引起，是铜中毒常见的形式，但是中毒症状是急性的，是由于肝脏中的铜突然释入血流所致。当肝铜蓄积到一定程度后，便释放大量铜进入血液，血铜浓度迅速提高并进人红细胞和排人尿液。     

绵羊慢性铜中毒的诊治

铜作为生物机体必需的微量元素之一，对维持机体的生理功能和促进生长发育起着十分重要的作用。然而，当机体摄人过量的铜，或是钼和硫等元素含量明显减少，以及肝细胞受到损害之后，均易引起铜在体内特别是肝脏的大量蓄积，从而引发铜中毒。铜中毒是由于动物摄食铜过多而引起的一种以腹痛、腹泻、肝功能异常和贫血为特征的一种中毒性疾病。各种家畜对铜的敏感程度不相同，其中绵羊对铜最敏感。慢性铜中毒早期临床表现不明显，以黄疸和血红蛋白尿为临床特征，家畜常因诊断和治疗不及时而死亡，对畜牧业的危害很大。     

猪铜中毒的诊治

猪发生铜中毒主要是因为摄入了过量的铜所致,病猪会表现腹痛、腹泻、肝功能异常和贫血等症状,属于猪常见的中毒性疾病。在养猪生产中硫酸铜是常用的饲料添加剂,如果添加量过多或混合不均匀,以及猪采食喷洒含铜农药的牧草等情况,都会使猪发生铜中毒。1患病表现铜中毒患猪精神较差,食欲减少或丧失食欲,被毛粗乱。     

实验性雏鸡铜中毒的病理学研究

选用1日龄艾维菌肉鸡180只随机分为3组，分别以对照日粮（Cu 11．97mg／kg）、铜中毒Ⅰ组日粮（Cu 650mg／kg）和铜中毒Ⅱ组日粮（Cu 850mg／kg）饲喂6周，以实验病理学方法系统研究了铜中毒对雏鸡组织器官和某些血液指标的影响。2个铜中毒组在试验的第2、3周先后出现临床症状；铜中毒Ⅱ组雏鸡的发病率和死亡率高于铜中毒Ⅰ组。病理形态学观察，2个铜中毒组的病变基本一致，表现为肌胃角质层增厚、龟裂，肠绒毛裸露断裂，伴有坏死；肝细胞脂肪变性；肾小管上皮细胞变性，坏死脱落；淋巴免疫器官体积缩小、重量减轻、淋巴细胞数量减少。2个铜中毒组雏鸡血清谷草转氨酶（AST）活性显著升高，红细胞数量、血红蛋白含量显著降低（P〈0．05或P〈0．01）。表明，雏鸡在生长发育的2～6周对高剂量铜较为敏感，毒性损坏的靶器官是肝、肾、胃肠道和淋巴免疫器官，铜中毒导致雏鸡组织器官受损、功能障碍及免疫功能低下，最终导致发病、死亡。     

家畜铜中毒研究进展

铜中毒是由于家畜摄食铜过多,或因肝细胞损伤,铜在肝脏等组织中大量蓄积,而突然释放进入血液循环所引起的一种重金属中毒性疾病。在生产中,家畜铜中毒屡见发生。文章归纳了铜中毒的发病特点和发病原因;总结了铜中毒的3 种发病机理,铜中毒的保护机制,铜与氧自由基的产生机制,铜毒理;论述了铜中毒的诊断依据、诊断指标和诊断方法;提出了铜中毒的综合性预防措施、治疗原则和治疗药物。为铜中毒病的诊断和防治提供了理论参考。     

应用DNA标记物C04107诊断犬铜中毒

美国科学院将卫星ＤＮＡ标记物Ｃ０４１０７连接在伯林顿狗铜中毒基因位点上，用于检测该疾病的等位基因，本试验将该标记物用于该病的诊断，发现该技术对于防治英国伯林顿狗铜中毒病具有重要意义，将这一标记物用于曾经肝组织活检为铜中毒阳性狗的诊断，得出了铜中毒阴性的结果，经重新肝组织活检证实被检狗确实为铜中毒阴性，证明应用卫星ＤＮＡ标记物Ｃ０４１０７做出的诊断结果是正确的。     

一起绵羊铜中毒的诊断

铜中毒是由于家畜摄食铜过多，或因肝细胞损伤，铜在肝脏等组织中大量蓄积，而突然释放进入血液循环所引起的一种重金属中毒性疾病。铜作为生物机体必需的微量元素之一，对机体的生理功能和生长发育起着十分重要的作用。适量的铜可刺激动物生长，提高饲料的利用率。然而，当机体摄入过量的铜，     

养羊生产应注意铜中毒

铜是动物机体不可缺少的必需微量元素之一．如动物长期多次或一次大量食人含铜的饲料往往发生严重溶血及消化、泌尿系统受损的中毒性疾病．铜中毒常见于羊、犊牛，以羊敏感，尤其是绵羊。笔者就生产中所遇到的铜中毒介绍给大家，以引起对该中毒性疾病足够的重视。     

反刍动物铜中毒的诊断与防治

铜中毒是由于动物摄入过量的铜盐而引起中毒的疾病，以绵羊最为敏感，牛次之。绵羊、犊牛1次性摄入铜20～100mg／kg，成年牛200～800mg／kg，便可引起急性铜中毒，而长期超量摄入铜也可以引起蓄积性中毒。现将反刍动物铜中毒的诊治方法介绍如下，供参考。     

猪铜中毒的诊治

在畜牧业生产中，家畜铜中毒屡有发生。笔者介绍了猪铜中毒病的诊断、治疗及预防方法。     

Taxus sp. intoxication in three Francois' langurs (Trachypithecus francoisi).

Three Francois' langurs (Trachypithecus francoisi) were found dead, without previous clinical signs, over a 48-hour period at a zoological institution after transfer to a new exhibit. A hybrid yew shrub (Taxus baccata X T. cuspidata) was found in close proximity to the exhibit perimeter fence. Despite clinical suspicion of yew intoxication, thin-layer chromatography performed on gastric contents was negative. However, microscopic examination of gastric contents revealed multiple yew fragments, and taxine alkaloids were detected by gas chromatography and mass spectrometry of the gastric contents to confirm yew intoxication. Acute death of the animals prevented treatment. The fourth langur in the collection survived, most likely because of its low rank in the troop's hierarchy, with a suspected small amount or none of the plant ingested. To the authors' knowledge, this case report is the first yew intoxication documented in a nonhuman primate species. Taxus spp. intoxication is an often fatal condition reported in domestic animals and humans. In comparison with these species, mortality appeared delayed in the Francois' langurs, most likely because of their unique gastrointestinal anatomy, with both foregut and colonic fermentation. Plant intoxication should be a differential diagnosis when multiple acute deaths are observed after recent introduction to a new enclosure.     

Haemolytic crisis in sheep as a result of chronic exposure to copper

Usually practicing veterinarians and animal keepers have to deal with inadequate supplementation of copper which causes deficiency diseases. However, instead of curing, the consequential intake of copper is likely to cause copper intoxication. Copper poisoning is observed particularly frequently, in sheep--the most sensitive domestic animal to copper toxicity. In most cases, sheep undergo chronic exposure to copper causing liver necrosis and resulting in massive haemolysis, haemoglobinuria and eventually in renal failure. The observed symptoms have an acute character and a set of them is called haemolytic crisis. The pathogenesis, signs and diagnosis of this syndrome are described in this article.     

Botulism poisoning in cattle,a case report,diagnosis and prevention

On a dairy farm 22 animals die in 14 days. After 10 days the clinical diagnosis is confirmed: clostridium botulinum type D intoxication. The clinical, diagnosis, therapy and prevention are discussed.     

X-ray microanalysis of liver and kidney in copper loaded sheep with and without thiomolybdate administration

The distribution of elements in the cells of the liver and kidney of normal sheep, of sheep chronically intoxicated with copper and in sheep given copper and thiomolybdate was studied by atomic absorption spectrophotometry, electron microscopy and electronprobe X-ray microanalysis. Copper concentrations were increased in the liver and kidney during the pre-haemolytic and haemolytic stages of the disease. In addition iron concentrations were markedly increased in the kidney during haemolysis. Copper and molybdenum concentrations were increased in the kidney of sheep receiving copper and thiomolybdate or thiomolybdate alone. By electronprobe X-ray microanalysis at the pre-haemolytic and haemolytic stages, copper together with small amounts of calcium and chromium were found in lysosomes of liver cells. In addition, in animals killed during haemolysis, high concentrations of iron were found in apical lysosomes of kidney proximal tubule cells. Copper and molybdenum were found in apical lysosomes of kidney tubule cells in animals given copper and thiomolybdate or thiomolybdate alone. The accumulation of copper with molybdenum and sulphur in the lysosomes of thiomolybdate treated copper intoxicated animals was demonstrated for the first time and may indicate the sequestration within lysosomes of a copper-molybdenum-protein complex.     

Veterinary and sanitary expertise in the USSR on the intoxication of animals with carbamate pesticides]

Pigs, sheep and rabbits were given carbamates per os. The animals were slaughtered one to thirty days after application. The examination of the slaughtered animals and meat was supplemented by determining the residues of carbamates in the meat and by physico-chemical, bio-chemical and bacteriological examinations. In the case of sevin, TMTD and/or zineb intoxication, pigs and sheep may be slaughtered after 20 to 30 days and rabbits seven to 12 days after intoxication. Meat containing sevin, TMTD and/or zineb may not be used for human consumption. After long-term storage of meat in freezing units and two-hour boiling the substance in the meat is not destroyed. From the veterinary and hygienic aspect the meat of the intoxicated animals may be used only after a complex examination.     

Sodium monofluoroacetate (Compound 1080) poisoning in dogs

Sodium monofluoroacetate (Compound 1080) is a widely used pesticide for control of feral animals such as the fox. Accidental poisoning of domestic animals occurs despite strict regulations on 1080 usage. Dogs are particularly susceptible to the toxin. The mechanism of 1080 toxicity, susceptibility of target and non-target species, persistence of 1080 in the environment and risk of accidental poisoning are discussed. Particular emphasis is placed on 1080 toxicity in the dog. Early recognition of intoxication is most important for prognosis and relies upon characteristic clinical signs and diagnostic findings. The treatment of 1080 intoxication remains a challenge with no proven antidotes. However, there are possible benefits from monoacetin, acetamide, calcium salts, colestipol, activated charcoal, peritoneal dialysis, sodium bicarbonate, neurotransmitter modulators and four-methylpyrazole. A recommended treatment protocol for 1080 toxicosis in dogs is included. Safety measures such as the use of wire dog muzzles and investigating alternatives to 1080 in pest control programs may be the key to reducing the incidence of future accidental poisonings.     

Residues of dimethoate in the liver and AchE activity in blood of rats after exposure to dimethoate, and dimethoate and pyrantel embonate

The study was aimed at determining the dimethoate residues in the liver and acetylcholinesterase (AChE) activity in blood of rats exposed to dimethoate (individual intoxication), and dimethoate and pyrantel embonate (simultaneous intoxication). The experiment was carried out in two stages where various doses of preparations and exposure manners were used. In the first stage of the experiment, dimethoate (1/25 LD50) was administered to animals per os for 28 days, and pyrantel embonate (1/2 LD550) twice, i.e. on the day 14th and 28th. In the second stage, dimethoate was administered for 5 days (1/10 LD50), and pyrantel embonate (1/5 LD50) on day 3, 4 and 5 from the beginning of dimethoate intoxication. The short presence of the dimethoate residues in the liver of the animals examined was found until the 2nd day after 28-day intoxication (1/25 LD50) and until 14th day after 5-day intoxication (1/10 LD50), however, a distinct decrease in this insecticide residues in the liver of (analysed groups of) rats occurred between the 3rd hour and the 2nd day after exposure. Dimethoate in both applied doses significantly reduced AChE activity in blood. After application of the higher dose, the inhibition of AChE was more pronounced, and the return of its activity to physiological values lasted considerably longer. Co-administration of pyrantel embonate and dimethoate, slightly influenced changes of the parameters analysed, which have been dependent not only on a dose and manner of pyrantel application but also on time which lapsed from exposure.     

Animal nutrition for veterinarians--recent cases of clinical disorders in horses after intake of ionophore-containing feed

Anamnesis and clinical signs of horses form five different stables after ingestion of ionophores are reported and techniques of feed examination are described. Within a few hours or days after feeding of new types or batches of concentrates horses fell ill. They showed colic-like symptoms with intense sweating and ataxia. Most of the sick animals died within a short time span. Samples of the concentrates were analysed and different types and amounts of ionophores were detected. In four cases contamination by monensin in concentrations of less than 5 mg to 679 mg/kg feed were found. One feed sample contained monensin (8.8 mg/kg feed) as well as salinomycin (67.3 mg/kg feed). In one case lasalocid (7.9 mg/kg feed) was present. One horse from the stable where animals had obtained concentrates containing monensin (679 mg/kg feed) was necropsied. Typical signs of monensin intoxication with severe myocardial degeneration were found. Veterinarians should be alert to this rare but severe intoxication of horses.     

Long‐term assessment of horses and ponies post exposure to monensin sodium in commercial feed

Reasons for performing study: Acute monensin intoxication in equids is well described; however, the long‐term effects of sublethal intoxication and ability to return to previous use are less well understood. Long‐term observations may allow improved estimation of prognosis in cases of sublethal intoxication. Objectives: To assess horses and ponies exposed to sublethal amounts of monensin for evidence of chronic sequelae and ability to return to prior/intended use. Methods: Twenty‐nine horses and 8 ponies were assessed utilising serum biochemistry, treadmill exercise stress testing, electrocardiography, and pre‐ and post exercise echocardiography ≥6 weeks after ingestion of monensin‐contaminated feed. Animals with evidence of monensin‐induced cardiomyopathy were re‐examined after a period of rest of ≥11 months. Follow‐up information was obtained by owner telephone interview ≥52 months after exposure. Results: During resting echocardiography, 11 animals had reduced/low‐normal left ventricular fractional shortening (FS); an increase in FS in 8 of these animals was measured ≥11 months later. Six animals had reduced or low‐normal FS during post exercise echocardiography. Two horses had ventricular premature depolarisations during exercise. Follow‐up information was available for 35 animals: 21 returned to athletic/reproductive use, 13 were retired immediately and one died. Mean FS increased significantly (P<0.001) between initial and second examination in 15 animals that underwent resting echocardiography on 2 occasions. Conclusions: Some equids exposed to sublethal doses of monensin may not develop permanent myocardial disease and a return to athletic/reproductive use is possible. Potential relevance: Exercise stress testing, echocardiography and electrocardiography may be useful for detection and monitoring of cardiac dysfunction in equids exposed to monensin and determining whether a return to athletic/reproductive use is possible.     

毒鼠强中毒的研究进展

毒鼠强是目前应用最广、毒性最强的灭鼠药。因误食或环境污染或人为投毒引起的人和动物中毒事件频繁发生 ,在我国已禁止使用 ,但由于其灭鼠效果好 ,故屡禁不止。毒鼠强为神经毒性毒物 ,致惊厥作用强烈 ,临床中毒者多表现典型颅脑损害症状。分析检验毒鼠强时 ,GC/NPD法灵敏度高 ,快速化学检测方法简便快捷 ,适用于现场检测。洗胃 ,控制抽搐、抗惊厥以及血液净化是有效的治疗措施。文章从理化特性、中毒症状、检验方法、诊断及治疗等方面综述了毒鼠强中毒的最新研究成果 ,以提高人们对毒鼠强中毒事件的认识和处置能力