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1.
Monensin toxicosis was induced in lambs by either a single oral dose of 12 mg/kg or six daily doses of 8 mg/kg. Clinical signs of toxicosis consisted of depression, dyspnea, stiffness of gait, reluctance to move, and recumbency. Serum creatine phosphokinase activity was increased. Samples of skeletal and cardiac muscle were obtained over a six-day period and examined by light and electron microscopy. Light microscopic changes in cardiac and skeletal muscles consisted initially of vacuolation and intracellular edema of muscle cells followed by segmental necrosis. Interstitial fibrosis was present on days 5 and 6 postexposure. Muscle fiber necrosis was more severe in skeletal than cardiac muscles and most severe in sheep given 8 mg/kg of monensin daily. Macrophages were seen only in areas of severe necrosis. The earliest ultrastructural change was severe swelling of mitochondria. Secondary changes consisted of lipid accumulation and myofibrillar alterations. Myoblast proliferation was present as early as four days after initial exposure to monensin.  相似文献   

2.
Dried Nerium oleander leaves at single lethal dose of 110 mg/kg body weight were administered orally to six native male sheep. Clinical signs of toxicosis in sheep began to appear about 30 min after receiving the oleander and included decrease of the heart rate followed by cardiac pauses and tachyarrhythmias; ruminal atony, mild to moderate tympany, abdominal pain, polyuria and polakiuria. Electrocardiography revealed bradycardia, atrio-ventricular blocks, depression of S-T segments, ventricular premature beats and tachycardia, and ventricular fibrillation. Five sheep died within 4-12 h and one survived. At necropsy there were varying degrees of haemorrhages in different organs and gastroenteritis. Histopathological examination of tissue sections revealed myocardial degeneration and necrosis, degeneration and focal necrosis of hepatocytes, necrosis of tubular epithelium in kidneys, oedema in the lungs, and ischemic changes in the cerebrum.  相似文献   

3.
Although the incidence of lead toxicosis in small animals continues to decrease, it remains a significant malady. We have reviewed the literature of the past 45 years, which revealed 70 cases involving cats. Sources, signs, diagnosis, pathology and treatment of feline lead toxicosis are reviewed. In 84% of these cases the source of lead was old paint usually from home renovation. The most common signs in cats are anorexia, vomiting, and seizures. The younger individuals seem more likely to show CNS signs. Since signs are often vague, lead toxicosis may be significantly under diagnosed in cats. The gold standard of diagnostic tests is blood lead concentration, although it does not necessarily correlate with total body burden of lead or with metabolic effects including clinical signs. Diagnostic tests including erythropoietic protoporphyrin (EPP), urine aminolevulinic acid, and others are discussed. Gross findings on necropsy are few and include a yellow-brown discoloration of the liver often with a nutmeg-like appearance. Histological examination may reveal pathognomonic inclusion bodies in liver and renal tissues. Characteristic histological changes in the CNS include neuronal necrosis and demyelination. Treatment of lead toxicosis in cats, as in any species, involves removing the exposure, decontaminating the individual and the environment, supportive care and chelation therapy. The most recently available chelator is succimer (meso 2,3-dimercaptosuccinic acid). Succimer given orally is well tolerated and has a wide margin of safety. A high index of suspicion of lead toxicosis is warranted in cats since they often present with vague and non-specific signs. With any consistent history owners need to be asked about home renovation. Early diagnosis and treatment affords a good prognosis.  相似文献   

4.
A phalaris grass (Phalaris caroliniana) caused neurologic signs and lesions in cattle and sheep. The sheep were hyperexcitable and uncoordinated, with severe muscle twitching, stiff gait, and head nodding. The cattle were thin, nervous, and ataxic. One feature of chronic phalaris toxicosis in these cases was onset of signs weeks or months after removal of the animals from the forage.  相似文献   

5.
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.  相似文献   

6.
Staggers was diagnosed in sheep and cattle from the northern California coast. The diagnosis was made on the basis of history of ingestion of perennial ryegrass (Lolium perenne) stubble, clinical signs of transient ataxia, which was aggravated by stimulation, and nearly complete recovery after removal of ryegrass as the primary forage. Morbidity was high, but death did not occur in any affected animals. The toxic endophyte, Acremonium lolii, was in most lower leaf sheaths from the ryegrass. Injection of extracts of the ryegrass from affected farms into mice induced signs of toxicosis. Additionally, ryegrass from all 3 farms contained the tremorgenic mycotoxin, lolitrem-B.  相似文献   

7.
Three horses died as a result of eating grass hay containing summer pheasant's eye (Adonis aestivalis L.), a plant containing cardenolides similar to oleander and foxglove. A 9-year-old thoroughbred gelding, a 20-year-old appaloosa gelding, and a 5-year-old quarter horse gelding initially presented with signs of colic 24-48 hours after first exposure to the hay. Gastrointestinal gaseous distension was the primary finding on clinical examination of all three horses. Two horses became moribund and were euthanatized 1 day after first showing clinical signs, and the third horse was euthanatized after 4 days of medical therapy. Endocardial hemorrhage and gaseous distension of the gastrointestinal tract were the only necropsy findings in the first two horses. On microscopic examination, both horses had scattered foci of mild, acute myocardial necrosis and neutrophilic inflammation associated with endocardial and epicardial hemorrhage. The third horse that survived for 4 days had multifocal to coalescing, irregular foci of acute, subacute, and chronic myocardial degeneration and necrosis. A. aestivalis (pheasant's eye, summer adonis) was identified in the hay. Strophanthidin, the aglycone of several cardenolides present in Adonis spp., was detected by liquid chromatography-mass spectrometry-mass spectrometry in gastrointestinal contents from all three horses. Although Adonis spp. contain cardiac glycosides, cardiac lesions have not previously been described in livestock associated with consumption of adonis, and this is the first report of adonis toxicosis in North America.  相似文献   

8.
Netobimin (coded SCH 32481, Schering Corporation), a new broad-spectrum anthelmintic having both fasciolicidal and nematocidal properties was evaluated for efficacy against mature Fasciola hepatica infections in sheep. The trial was conducted with 30 cross-bred spring lambs, each experimentally infected with 250 F. hepatica metacercariae. A single treatment of netobimin was administered at 17 weeks post-infection (PI) by oral drench at 7.5 or 20 mg kg-1 body weight while 10 animals remained as untreated controls. At necropsy (either 1 or 2 weeks post-treatment), the mean number of adult flukes recovered from the control, 7.5 and 20 mg kg-1 groups were 94.7, 35.9 and 8.8, respectively. The resulting efficacies were 62% (P less than or equal to 0.05) and 90.7% (P less than or equal to 0.01), respectively. No clinical signs of fascioliasis were noted in any sheep during the trial. No signs of toxicosis nor any adverse reactions to the drug were observed.  相似文献   

9.
The purpose of this study was to review the medical records of dogs that were either suspected or known to have ingested large doses of pimobendan and to describe the clinical signs associated with pimobendan toxicosis. The database of Pet Poison Helpline, an animal poison control center located in Minneapolis, MN, was searched for cases involving pimobendan toxicosis from Nov 2004 to Apr 2010. In total, 98 cases were identified. Of those, seven dogs that ingested between 2.6 mg/kg and 21.3 mg/kg were selected for further evaluation. Clinical signs consisted of cardiovascular abnormalities, including severe tachycardia (4/7), hypotension (2/7), and hypertension (2/7). In two dogs, no clinical signs were seen. Despite a wide safety profile, large overdoses of pimobendan may present risks for individual pets. Prompt decontamination, including emesis induction and the administration of activated charcoal, is advised in the asymptomatic patient. Symptomatic and supportive care should include the use of IV fluid therapy to treat hypotension and address hydration requirements and blood pressure and electrocardiogram monitoring with high-dose toxicosis. Practitioners should be aware of the clinical signs associated with high-dose pimobendan toxicosis. Of the dogs reported herein, all were hospitalized, responded to supportive care, and survived to discharge within 24 hr of exposure.  相似文献   

10.
This is the first study of Sarcocystis-induced abortion in sheep. Eleven pregnant ewes were experimentally inoculated with 50,000, 100,000, or 500,000 Sarcocystis ovicanis sporocytis from dogs. Eight ewes either aborted, died, or became moribund before term; they produced 15 fetuses, 11 of normal appearance and 4 necrotic. No evidence of intrauterine transmission was obtained. All infected ewes became anemic, inappetent, and lost weight. Ewes inoculated with the greatest numbers of sporocysts exhibited the most striking signs of acute illness. At necropsy of acutely ill ewes the heart was the most severely affected organ, appearing nearly black as a result of hemorrhagic pancarditis. Less hemorrhage was seen in the kidney, liver, spleen, and skeletal muscles. Microscopically, schizonts were found in capillary endothelial cells of most organs 24 to 33 days after inoculation. Ewes surviving the acute illness appeared generally unthrifty and exhibited the additional signs of wool breaking, and nervous disturbances. At postmortem, the heart and kidneys of these ewes were moderately hemorrhagic, and the adrenal glands and mesenteric lymph nodes were enlarged. Microscopically, sarcocysts were found in the heart, diaphragm esophagus, tongue, skeletal and eye muscles, cerebellum, and cerebrum.  相似文献   

11.
Pathology of experimentally-induced, acute toxoplasmosis in macropods   总被引：1，自引：0，他引：1  
SUMMARY Thirteen Tammar wallabies (Macropus eugenii) were dosed orally with 500, 1000 or 10 000 oocysts of Toxoplasma gondii, as part of a vaccination trial. Eleven animals died of acute toxoplasmosis 9 to 15 days after challenge. The lesions were similar in all animals, consisting of foci of necrosis and inflammation in the intestines, lymphoid tissue, adrenal cortex, heart, skeletal muscle and brain, and severe generalised pulmonary congestion and oedema. Free and intracellular tachyzoites of Toxoplasma were associated with the lesions. The remaining 2 animals had shown no signs of disease when euthanased four months after challenge. Small, focal, non-suppurative inflammatory lesions were seen in brain, heart and skeletal muscle of these animals and chronic Toxoplasma infection was confirmed by mouse inoculation.  相似文献   

12.
Antidotal effects of the 2 antioxidants butylated hydroxyanisole (BHA) and ethoxyquin (EQ) were evaluated in bitterweed (Hymenoxys odorata DC) toxicosis in sheep. Bitteerweed contains a toxic sesquiterpene lactone, hymenoxon, the toxicity of which is reduced by cysteine. Both BHA and EQ are known to induce hepatic glutathione production in rodents. Treatment of sheep with EQ (2.5 g/sheep/day for 9 days before poisoning) gave significant protection from toxic doses of bitterweed, but the protective effect of BHA was insignificant. Of 6 sheep given EQ in the feed, 5 survived 7 doses of bitterweed (4 g/kg/day or higher for 7 days), whereas 5 of 7 controls and 4 of 7 sheep given feed with added BHA died. The added EQ in the feed decreased the serum alkaline phosphatase activity and total protein, albumin, and calcium concentrations. Seemingly, EQ is the first protective agent with field application potential for bitterweed toxicity.  相似文献   

13.
本研究利用不连续聚丙烯酰胺凝胶电泳法对绵羊的８种组织器官ＬＤＨ同工酶的分布及相对活性进行了分析测定。比较ＬＤＨ同工酶的酶谱特征。结果表明，绵羊的ＬＤＨ同工酶分布特征不同于其它动物，其相对活性有显著差异。骨骼肌中ＬＤＨ５活性比ＬＤＨ１强，Ｍ亚基比例大于Ｈ亚基；肝脏和心脏中ＬＤＨ１的活性最强。  相似文献   

14.
During the 5-year period from January 1, 1990, to December 31, 1995, 887 diagnoses of metal toxicosis in domestic animals and wild birds were documented at the Veterinary Laboratory Services Branch of the Ontario Ministry of Agriculture, Food and Rural Affairs. Most of these cases involved cattle, sheep, and birds. Lead toxicosis was diagnosed in 399 cases, copper toxicosis in 387, zinc toxicosis in 49, mercury toxicosis in 44, iron toxicosis in 4, and selenium in 4 cases. Trends in species affected and sources of metals are discussed.  相似文献   

15.
Dichlorvos was applied as spray at 1 and 2% concentrations daily for a period of 28 and 21 consecutive days, respectively to buffalo calves. Animals sprayed with 1% dichlorvos displayed mild to moderate clinical signs of toxicosis during the 4th week of exposure. The higher concentration (2%) produced clinical signs of poisoning after 12-16 applications, and was lethal to one of three animals. Daily spraying of dichlorvos at both concentrations inactivated erythrocyte cholinesterase (ChE) (15-21%), plasma ChE (17-20%) and serum carboxylesterase (5-10%) within 3 days. The extent of inhibition of esterases was increased with repeated treatment and maximal inhibition of erythrocyte ChE (80-89%), plasma ChE (81-91%) and serum carboxylesterase (33-54%) with 1 and 2% concentrations was observed on the 28th and 21st day after start of application, respectively. In surviving animals, blood esterases remained inactivated to the extent of 14-65% on the 14th day after the termination of treatment. Dichlorvos at both concentrations significantly (P less than 0.01) elevated the serum levels of aspartate aminotransferase, alanine aminotransferase, acid phosphatase and alkaline phosphatase. The activities of these enzymes in surviving animals recovered to control values within 14 days after the final application of dichlorvos.  相似文献   

16.
Tryptamine alkaloid toxicosis (Phalaris staggers) was diagnosed in feedlot sheep. Clinical signs of toxicosis, which were exacerbated by excitement, included gait abnormalities, muscular tremors, nystagmus, and convulsions. An estimated 8% of the most severely affected lambs had clinical signs of toxicosis. Gross lesions detected in the brain of affected lambs consisted of focal gray-green discoloration in the brain stem and thalamus; these areas had microscopic evidence of intraneuronal pigment accumulation. Brain specimens obtained at slaughter indicated that 60% of the lambs had lesions consistent with tryptamine alkaloid toxicosis. Tryptamine alkaloids were found in low concentrations in the feed. Lambs exposed to these feeds had higher death losses than those that were not exposed to the feeds. Cobalt concentration in the feed was higher than that previously reported to be associated with Phalaris staggers.  相似文献   

17.
From 1986 to 1989, 5 desert bighorn sheep (3 Ovis canadensis mexicana and 2 O c nelsoni), ranging in age from 2 to 3 years, were exposed to a flock of exotic wild and domestic sheep to potentially achieve naturally acquired pneumonia. Pasteurella multocida was isolated from nasal samples from 4 of 6 sheep randomly sampled from the flock. Bighorn sheep were exposed individually and each exposure period was a trial. Treatment before and after exposure varied and included combinations of alpha interferon, antibiotics, anti-inflammatory drugs, and vaccines. Treatments were chosen on the basis of recommendations of others for treating pneumonia in desert bighorn sheep as well as our own experience in sheep and cattle. Regardless of treatment used, bighorn sheep in trials 1 to 4 developed signs of pneumonia within 10 to 14 days of exposure. Bighorn sheep in trials 1 to 3 died within 11 to 17 days of initial exposure. In trial 4, the bighorn sheep was isolated from the carrier sheep for treatment of pneumonia on day 14 and died on day 30. Pasteurella multocida was isolated from lung tissue in 3 of the 4 bighorn sheep. On the basis of results of trials 1 to 4, a more in depth clinical study was conducted in trial 5. Nasal and blood specimens were collected prior to and during trial 5 for bacteriologic culturing and serologic testing for bovine viral diarrhea virus, infectious bovine rhinotracheitis, parainfluenza-3 virus, and respiratory syncytial virus.(ABSTRACT TRUNCATED AT 250 WORDS)  相似文献   

18.
Acute monensin toxicosis in sheep: light and electron microscopic changes   总被引：2，自引：0，他引：2  
Monensin was administered orally to 3 sheep at dosages of 12 (the LD50), 16, and 24 mg/kg of body weight, respectively. Clinical signs of monensin toxicosis were observed in the sheep in 24 to 36 hours of administration. Clinical signs included CNS depression, anorexia, diarrhea, and stiffness. Increased serum creatine phosphokinase and aspartate aminotransferase activities identified possible muscle damage. Sheep were euthanatized at 54 hours after dosing; at necropsy, there were skeletal muscle hemorrhages, pale myocardium, and pulmonary edema. Ultrastructural lesions were in the liver, diaphragm, and myocardium; diaphragm and myocardium were most severely affected. Mitochondrial swelling and cristolysis, swollen sarcoplasmic reticulum, and disruption of myofibrillar architecture were prominent. These ultrastructural changes are consistent with the hypothesis that monensin causes muscle cell necrosis due to its ionophorous properties and disruption of cellular Na+:Ca2+ balance. It is proposed that this upset of normal ionic processes allows increased intracellular calcium, which directly leads to the functional and structural mitochondrial changes observed.  相似文献   

19.
After very hot summer, 22 sheep from 5 different flocks consisting of approximately 150-200 animals each were diagnosed with facial eczema in September 2005, in southwest Turkey. Photophobia, corneal opacity, severe ulcers of the facial skin, especially localized around the eyes and mouth, and 3% mortality were the most prominent clinical symptoms. GGT levels of the animals were very high and varying between 261- 328 U/l. While the activities of ALT and total bilirubin were elevated and AST was normal in affected sheep. Total bilirubin level was higher than normal. Seven of the 22 sheep were euthanatized and necropsy was performed on all of these animals. Severe icterus, hepatomegaly, enlarged gallbladder, congestion of mesenteric vessels were the common necropsy findings. Histopathological changes of the liver included necrosis of the hepatocytes, cholangiohepatitis characterized by mononuclear inflammatory cell infiltrate in the portal area and mild to severe fibrosis around bile ducts. A diagnosis of sporidesmin toxicosis was made based on the histopathology of the livers, the elevation in liver enzymes, and the development of cutaneous lesions consistent with photosensitization and high spore counts in the ruminal contents. Surviving sheep were treated with procaine penicillin + dihidrostreptomycin sulfate, multivitamin complexes and flunixin meglumine. Additionally, zinc sulphate was also given at a dose of 6 gr per 100 lt drinking water for 28 days. All treated sheep recovered. Pasture spore counts were between 96,300- 267,500 spores/g grass.  相似文献   

20.
The bacteriologic, immunologic, and clinical responses of 3- to 4-month old Holstein-Friesian calves to experimental exposure with Moraxella bovis type 10900 has been investigated. After u.v. radiation and intraconjunctival exposure with 1.9 × 107 microorganisms, each eye of 16 calves exhibited signs of blepharospasm, photophobia, and increased lacrimation. Bacteria were recovered from exposed eyes for 2–7 consecutive weeks before maximal clinical response occurred. The severity of the cases varied from eyes that exhibited mild signs to severe clinical cases with profuse lacrimation, conjunctival swelling, corneal opacity, and ulceration. By 70 days after exposure, M. bovis could not be recovered from any conjunctival swabs, and clinical signs were not observed. Four non-exposed control animals did not develop clinical signs nor was M. bovis recovered from conjunctival swabs.Lacrimal secretions collected at the time of and 1 week after maximal clinical response had significantly elevated levels of total protein as compared to those collected 3, 2, and 1 week before, and 2 and 3 weeks after maximal clinical response. A passive hemagglutination test, using tanned formalized sheep erythrocytes sensitized with M. bovis sonicate antigen, detected antibody in lacrimal secretions from 22 of 32 eyes. The appearance of specific antibody in lacrimal secretions correlated with the amelioration of clinical signs and the decline in numbers of M. bovis microorganisms recovered from conjunctival swabs.  相似文献   

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